FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Gene: Dmel\N
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General Information
Symbol
Dmel\N
Species
D. melanogaster
Name
Notch
Annotation Symbol
CG3936
Feature Type
FlyBase ID
FBgn0004647
Gene Model Status
Stock Availability
Gene Summary
Essential signaling protein which has a major role in many developmental processes (PubMed:3935325). Functions as a receptor for membrane-bound ligands Delta and Serrate to regulate cell-fate determination (PubMed:10935637, PubMed:12909620, PubMed:15620650, PubMed:18243100). Upon ligand activation, and releasing from the cell membrane, the Notch intracellular domain (NICD) forms a transcriptional activator complex with Su(H) (Suppressor of hairless) and activates genes of the E(spl) complex (PubMed:7671825). Regulates oogenesis, the differentiation of the ectoderm and the development of the central and peripheral nervous system, eye, wing disk, muscles and segmental appendages such as antennae and legs, through lateral inhibition or induction (PubMed:11719214, PubMed:12369105, PubMed:3935325). Regulates neuroblast self-renewal, identity and proliferation through the regulation of bHLH-O proteins; in larval brains, involved in the maintenance of type II neuroblast self-renewal and identity by suppressing erm expression together with pnt; might also regulate dpn expression through the activation of the transcriptional regulator Su(H) (PubMed:18342578, PubMed:20152183, PubMed:21262215, PubMed:23056424, PubMed:27151950, PubMed:28899667). Targeted for ESCRT-mediated endosomal sequestration and lysosomal degradation by various E3 ubiquitin ligases to regulate the Notch signaling pathway (PubMed:17084358, PubMed:22162134, PubMed:33349255). Can undergo ligand-dependent and non-canonical ligand-independent activation (PubMed:22162134). Ligand-independent activation is dependent on endosome acidification and probably occurs in late endosomes or lysosome (PubMed:23178945). Ectopic ligand-independent activation occurs when disruption of the endolysosomal pathway, particularly of the ESCRT-III complex, prevents sequestration of the receptor in intraluminal vesicles of multivesicular bodies (PubMed:17084357, PubMed:17084358, PubMed:17088062, PubMed:23178945). (UniProt, P07207)
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Also Known As

Ax, spl, NICD, fa, Abruptex

Key Links
Genomic Location
Cytogenetic map
Sequence location
Recombination map
1-2
RefSeq locus
NC_004354 REGION:3134870..3172221
Sequence
Genomic Maps
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
Gene Ontology (GO) Annotations (129 terms)
Molecular Function (7 terms)
Terms Based on Experimental Evidence (6 terms)
CV Term
Evidence
References
inferred from direct assay
inferred from physical interaction with FLYBASE:htk; FB:FBgn0085451
inferred from physical interaction with FLYBASE:Ser; FB:FBgn0004197
inferred from physical interaction with FLYBASE:wry; FB:FBgn0051665
inferred from physical interaction with UniProtKB:Q9VLL3
inferred from physical interaction with FLYBASE:Su(H); FB:FBgn0004837
inferred from physical interaction with FLYBASE:shg; FB:FBgn0003391
inferred from physical interaction with FLYBASE:Su(dx); FB:FBgn0003557
inferred from physical interaction with UniProtKB:E1JHA6
inferred from physical interaction with UniProtKB:Q9Y0H4
inferred from physical interaction with FLYBASE:Nedd4; FB:FBgn0259174
inferred from direct assay
Terms Based on Predictions or Assertions (1 term)
CV Term
Evidence
References
Biological Process (106 terms)
Terms Based on Experimental Evidence (98 terms)
CV Term
Evidence
References
inferred from mutant phenotype
involved_in axon guidance
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with UniProtKB:Q9VQ56
inferred from mutant phenotype
inferred from mutant phenotype
involved_in chaeta development
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from direct assay
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
involved_in long-term memory
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:klg; FB:FBgn0017590
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from expression pattern
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from direct assay
inferred from genetic interaction with FLYBASE:nerfin-1; FB:FBgn0028999
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:Cdk9; FB:FBgn0019949
inferred from genetic interaction with FLYBASE:Abl; FB:FBgn0000017
involved_in oogenesis
inferred from mutant phenotype
inferred from direct assay
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:scrib; FB:FBgn0263289
inferred from mutant phenotype
inferred from genetic interaction with UniProtKB:P51023
inferred from genetic interaction with UniProtKB:P51023,UniProtKB:Q9VQ56
inferred from genetic interaction with UniProtKB:Q9VQ56
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
Terms Based on Predictions or Assertions (10 terms)
CV Term
Evidence
References
traceable author statement
involved_in dorsal closure
traceable author statement
involved_in lateral inhibition
traceable author statement
traceable author statement
traceable author statement
traceable author statement
Cellular Component (16 terms)
Terms Based on Experimental Evidence (16 terms)
CV Term
Evidence
References
inferred from mutant phenotype
inferred from mutant phenotype
located_in cell surface
inferred from direct assay
colocalizes_with cytoplasmic vesicle
inferred from direct assay
located_in cytoplasm
inferred from direct assay
located_in early endosome
inferred from direct assay
inferred from direct assay
inferred from mutant phenotype
located_in endosome
inferred from direct assay
colocalizes_with late endosome
inferred from direct assay
located_in late endosome
inferred from direct assay
colocalizes_with lysosome
inferred from direct assay
located_in membrane
inferred from direct assay
located_in nucleus
inferred from mutant phenotype
inferred from physical interaction with FLYBASE:Su(H); FB:FBgn0004837
Terms Based on Predictions or Assertions (1 term)
CV Term
Evidence
References
Protein Family (UniProt)
Belongs to the NOTCH family. (P07207)
Summaries
Pathway (FlyBase)
NOTCH SIGNALING PATHWAY CORE COMPONENTS -
The Notch receptor signaling pathway is activated by the binding of the transmembrane receptor Notch (N) to transmembrane ligands, Dl or Ser, presented on adjacent cells. This results in the proteolytic cleavage of N, releasing the intracellular domain (NICD). NICD translocates into the nucleus, interacting with Su(H) and mam to form a transcription complex, which up-regulates transcription of Notch-responsive genes. (Adapted from FBrf0225731 and FBrf0192604). Core pathway components are required for signaling from the sending cell and response in the receiving cell.
Gene Group (FlyBase)
CSL-NOTCH-MASTERMIND TRANSCRIPTION FACTOR COMPLEX -
The CSL-Notch-Mastermind transcription factor complex consisting of the CSL protein, Su(H), and mastermind (mam) protein, in complex with Notch intracellular domain (generated by ligand-stimulated N-cleavage), up-regulates transcription of Notch-responsive genes. (Adapted from FBrf0232880).
UNCLASSIFIED TRANSMEMBRANE RECEPTORS -
This group comprises transmembrane receptors that do not classify under other groups in FlyBase.
Protein Function (UniProtKB)
Essential signaling protein which has a major role in many developmental processes (PubMed:3935325). Functions as a receptor for membrane-bound ligands Delta and Serrate to regulate cell-fate determination (PubMed:10935637, PubMed:12909620, PubMed:15620650, PubMed:18243100). Upon ligand activation, and releasing from the cell membrane, the Notch intracellular domain (NICD) forms a transcriptional activator complex with Su(H) (Suppressor of hairless) and activates genes of the E(spl) complex (PubMed:7671825). Regulates oogenesis, the differentiation of the ectoderm and the development of the central and peripheral nervous system, eye, wing disk, muscles and segmental appendages such as antennae and legs, through lateral inhibition or induction (PubMed:11719214, PubMed:12369105, PubMed:3935325). Regulates neuroblast self-renewal, identity and proliferation through the regulation of bHLH-O proteins; in larval brains, involved in the maintenance of type II neuroblast self-renewal and identity by suppressing erm expression together with pnt; might also regulate dpn expression through the activation of the transcriptional regulator Su(H) (PubMed:18342578, PubMed:20152183, PubMed:21262215, PubMed:23056424, PubMed:27151950, PubMed:28899667). Targeted for ESCRT-mediated endosomal sequestration and lysosomal degradation by various E3 ubiquitin ligases to regulate the Notch signaling pathway (PubMed:17084358, PubMed:22162134, PubMed:33349255). Can undergo ligand-dependent and non-canonical ligand-independent activation (PubMed:22162134). Ligand-independent activation is dependent on endosome acidification and probably occurs in late endosomes or lysosome (PubMed:23178945). Ectopic ligand-independent activation occurs when disruption of the endolysosomal pathway, particularly of the ESCRT-III complex, prevents sequestration of the receptor in intraluminal vesicles of multivesicular bodies (PubMed:17084357, PubMed:17084358, PubMed:17088062, PubMed:23178945).
(UniProt, P07207)
Phenotypic Description (Red Book; Lindsley and Zimm 1992)
Ax: Abruptex (W.J. Welshons)
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Ax: Abruptex
From Mohr, 1932, Proc. Intern. Congr. Genet., 6th, Vol. 1: 190-212.
Homozygous females and males show shortened L5 vein, usually also L4, L2, and sometimes L3. Wings shortened, arched, and thin. Costal bristles clumped and frayed; costal veins thickened. Thorax shows midfurrow with rearranged hair directions; hairs on thorax and head fewer, with clear patches and streaks. Male genitalia often rotated. Ax/+ females show short L5 in half of the flies and sparse hair pattern on thorax. Lower temperature (19) markedly decreases expression, and higher temperature enhances it. Some Ax alleles enhance N expression in Ax/N heterozygotes, but others suppress the dominant N phenotype. For example, Ax/N8 approaches wild type in all characteristics. No wing-vein interruption in Ax/+ at 18 and 26, and enhancement by H occurs so that Ax/Y;H/+ and Ax/Ax;H/+ are nearly lethal at 26 (House, 1959, Anat. Record 134: 581-82). Ax/Ax;ciD/+ and Ax/Y;ciD/+ are lethal or nearly so at 26. At 22, males survive and show enhanced wing-vein interruption and more missing bristles. At 26, wing-vein interruption approaches 100% in Ax/+;ciD/+ (House and Lutes, 1975, Genetics 80: s42-43). Wing nicking is suppressed in Ax/N55e11 at 25, and Ax venation is weakly expressed; Ax/Ax;Dp(1;2)51b/+ shows weak Ax venation (Portin, 1975, Genetics 81: 121-33). Nearly lethal when reared at 29; temperature-sensitive period early pupa (Portin and Sir'n, 1976, Hereditas 84: 109-16). In heterozygotes of Ax with the recessives at Notch at 18 and 25, there is neither expression of the recessive nor Ax-type venation. At 29, only Ax/fano shows some weak expression of the recessive, and all heterozygotes except Ax/nd2 show some Ax venation (Portin, 1977, Hereditas 87: 77-84). Ax interacts with alleles Ax9, Ax59b, Ax71d, Ax16, and AxE2 (see appropriate entry). RK2 in males.
Ax1
Temperature-sensitive lethal; male viable at 25 but nearly lethal at 29. Ax1/AxE2 semilethal at 25 and lethal at 29. Temperature-sensitive period for lethality of Ax1 at beginning of pupal stage; of Ax1/AxE2 at end of third instar and into early pupal stage.
Ax9
Viable in both sexes but poorly fertile or sterile. Bristle loss and vein interruptions are more extreme at 29. Heterozygotes of Ax9 with Ax1 and AxE1 are viable, but Ax9 is inviable with Ax71d, Ax16, and AxE2 (negative complementation). The lethality associated with negative complementation is suppressed by 23 lethal Notch alleles as well as by alleles of Dl and mam (Xu, Rebay, Fleming, Scottgale, and Artavanis-Tsakonas). When heterozygous with N mutants, phenotypes of Ax and N tend toward normal, but there is temperature sensitivity for suppression of wing nicks (Foster, 1975; Portin, 1975). Ax9 complements every recessive visible on the Notch map at 18 to 29 (Portin, 1977, Hereditas, 87: 77-84); with Ax59b and Ax59d, it is semilethal. Negative complementation is eliminated by Dp(1;2)51b and results in a strong Ax phenotype (Portin, 1975). The fate map for negatively complementing heteroallelic Ax9/AxE2 suggests a focus of lethality in tissue close to hypodermal sites of central thoracic structures; in surviving gynandromorphs, negative complementation for morphological defects is autonomous (Portin, 1977, Genetics, 86: 309-19).
Ax16
Homozygotes resemble Ax1. Ax16 is less fertile than alleles AxE2, Ax71d, and Ax9 (Portin, 1975), and temperature sensitive for the bristle and wing effects of Ax (Foster, 1975). In heterozygotes with Notch, Ax is expressed and the Notch wing effect is enhanced (Foster, 1975; Portin, 1975). At 29, heterozygotes with N are lethal. In Ax16/N264-40 heterozygotes, the TSP for lethality is in the second instar, and for Ax-morphological effects, it is in the third instar (Foster, 1973, 1975). In heterozygotes with recessive visibles at Notch, all are complementary at 18 and 25; at 29, there are mild indications of noncomplementarity with nd and nd2 (Portin, 1977). Heteroalleles Ax16/AxE2 and Ax16/Ax71d are viable (Foster, 1975; Portin, 1975); Ax16/AxE1 is inviable (negative heterosis) and heterozygotes with Ax9 and Ax1 are lethal (negative complementation) (Foster, 1975; Portin, 1975), but Dp(1;2)51b restores viability (Portin, 1977). Heterozygotes with the lethal alleles Ax59b and Ax59d are lethal and mostly inviable upon the addition of Dp(1;2)51b (Portin, 1975, 1977).
Ax59b
Homozygotes and hemizygotes semilethal at 22; lethality approximates 100% at 25. Lethal in heterozygotes with N mutants but viable and fertile with recessive visibles at Notch. Ax59b/Ax59b; Dp(1;2)51b/+ are poorly viable and infertile, and mutant phenotype is enhanced. Ax59b/+; Dp(1;2)51b/+ females have diminished mutant expression compared to Ax59b/+ females which in turn are similar to males Ax/Y; Dp(1;2)51b/+. In heterozygotes with spl at 25, the eye is reduced in size but is larger than in spl/spl, and eye roughness varies from very mild to undetectable. The report by Welshons that Ax59b/spl did not express the split phenotype was an error caused by uncontrolled temperature variation. In cis heterozygotes, spl Ax59b/++, expression of split is enhanced compared to Ax59b/spl; the eyes are rough and reduced in size. No such enhancement is seen when fag is coupled to Ax59b, and in Ax59b/fag, the expression of the recessive is very mild and frequently nonpenetrant (Welshons, 1971). Ax59b is semilethal with Ax9 and lethal with alleles Ax16, AxE2, Ax71d, Ax1, and the addition of Dp(1;2)51b to heterozygotes of Ax59b with Ax9 and Ax1 restores viability (Portin, 1975). The temperature sensitivity of the Ax59b phenotype is strongest at 25; mutant expression decreases at both 18 and 29, with the least mutant expression at 29 (Portin, 1981, Hereditas 94: 93-98). At 18, there is complementarity with all recessive visibles at Notch and strong Ax expression in every case except when heterozygous with fag. At 29, all heterozygotes are noncomplementary with the exception of nd; Ax expression is diminished. At 29, homozygotes or hemizygotes with Dp(1;2)51b are more viable than at 18 or 25 (Portin, 1977). At 25, wing-vein interruption and bristle loss increases with an increased dose of the mutant gene (Portin, 1981, Hereditas 95: 247-51). Somatic crossing over yields twin spots on cuticular surface of flies, indicating that Ax59b is not a primary cell lethal (Portin, 1980).
Ax71d
Homozygous, viable, phenotype like Ax1. Viable with alleles AxE2 and Ax16, and lethal with Ax1 and Ax9 (negative complementation), but viability restored by Dp(1;2)51b. There is no obvious effect on the Notch phenotype in heterozygotes with N8 or N55e11, but Ax phenotype is expressed. In heterozygotes with AxE2, the mutant phenotype is weakly expressed; heterozygotes with lethal alleles Ax59b and Ax59d are lethal. Ax71d is complementary with recessive alleles at Notch at 18, 25, and 29. The mutant expression of Ax tends to increase with increasing temperature except that Ax71d/nd2 at 29 has no Ax expression.
Ax75c
Recessive lethal like alleles Ax59b and Ax59d. Ax75c/+ is temperature sensitive for pleiotropic effects; the variation in mutant expression with temperatures of 18, 25, and 29 resembles that of Ax59b and Ax59d with some variation in detail (Portin, 1981, Hereditas 94: 93-98). The Ax mutant phenotype increases with increasing dose of the allele (Portin, 1981, Hereditas 95: 247-51).
AxE1
AxE1/+ females at 20.5 have gaps in wing veins and a reduction in number of ocellar and postvertical bristles. Semilethal as hemizygote or homozygote. Heterozygotes AxE1/Ax9 are viable and phenotypically intermediate: AxE1/AxE2 and AxE1/Ax16 are inviable (negative heterosis). AxE1 is inviable with most N mutants, but heterozygotes with N264-103 (a temperature-sensitive mutant) survive at 22 but not at 29.
AxE2
Homozygous viable, phenotype like Ax1. Temperature sensitive for morphological phenotypes (Foster, 1975) but stable for viability (Portin and Siren, 1976). Viable in heterozygotes with N; Notch-wing phenotype is enhanced. At 18 and 25, complementary in heterozygotes with recessive alleles at Notch; at 29, spl and nd2 are weakly expressed (Portin, 1977, Hereditas 87: 77-94). Heterozygotes fano spl AxE2/+++ are like spl/spl with suppression of wing-vein gaps; fano++/+ spl AxE2 and +spl AxE2/+++ show mild expression of spl (Foster, 1975). AxE2 is viable with alleles Ax71d and Ax16; lethal with lethal alleles Ax59b and Ax59d and with AxE1, Ax9, and Ax1 (Foster, 1975; Portin, 1975), and the lethality with Ax1 is more pronounced at 29 (Portin and Sir'n). In AxE2/Ax1, the TSP for lethality is monophasic from the end of the third instar to early pupa (Portin and Sir'n, 1976). In AxE2/Ax9, the focus of lethality is close to hypodermal sites of ventral thoracic structures, and in surviving gynandromorphs, the negative interaction between alleles is autonomous (Portin, 1977, Genetics 86: 309-19).
AxJ14
Male lethal, mutant phenotype similar to Ax1. Lethality is covered by Dp(1;2)51b and Dp(1;2)w64d, and males with the duplication show the Ax phenotype. When lethality is covered by w+Y, males have normal wing venation but lack ocellar bristles. In heterozygotes with fal2, females survive exhibiting a strong Ax phenotype and rough eyes.
AxS (A. Schalet)
Male and female homozygotes lethal. AxS/+ males and females show sparse thoracic hairs. AxS/Ax similar to Ax/Ax, viability strongly reduced. AxS/NS is lethal. Not suppressed by su(Hw)2.
Axtsl
Ax phenotype 100% penetrant in heterozygotes at 18 and 29; homozygous lethal at 29 and semilethal at 18. Surviving homozygotes have a stronger Ax expression than in heterozygotes. Lethal with N mutants at 29 and semilethal with Ax59d. Ax in phenotype and complementary with recessive visibles at Notch at 18 and noncomplementary at 29.
Co: Confluens (W.J. Welshons)
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Co: Confluens
Edith M. Wallace, unpublished.
Veins irregularly thickened, especially toward tips, which are usually deltas and fused broadly to marginal vein. Stronger expression in males than in females. Co/N8 wild type except for slightly thicker L3 vein. Co/Ax like Ax/+. RK1A.
fa: facet (W.J. Welshons)
Facet mutants affect the texture of the eye and in some cases cause slight to moderate wing nicks. Until now some recessive mutations with wing nicking but with normal eye texture have been designated as alleles of fa based upon their not being complemented by N mutants; in this treatment their designations have been changed to nd: notchoid, since they fail to complement nd mutants and like nd alleles, they complement fa alleles. All fa alleles complement spl, another eye-texture mutant in the N locus.
fa1
Eyes of all males moderately rough owing to irregularity in size, shape, and arrangement of facets. Not dosage compensated; eyes of females less rough than those of males with about 10% overlap of wild type. Eye roughness of the females varies from nearly normal at 18 to marked at 29; pupal stage temperature sensitive (Shellenbarger and Mohler, 1975, Genetics 81: 143-62). Eye abnormality caused by overgrowth of secondary pigment cells, which compresses cones and causes overlying corneal facets to bulge (Waddington and Pilkington, 1942, DIS 16: 70). Wings have apical nicks in 0.25% of males and 0-5% of females. N/fa1 has rough eyes of fa1 as well as a Notch phenotype
fa3
Eyes equally rough in both sexes; wings not notched. Eyes rougher than in fa males but not glossy as in fag; heterozygotes fa3/fag are rough, not glossy (Welshons).
*fado-vg: facet-dominigene for vestigial
By itself, it is wild type. fado-vg/fa1 shows rough eye character of fa1. fado-vg/fado-vg; vg/+ produces some wing notching. Presumed by Goldschmidt to enhance dominance of vg and thus termed a "dominigene". RK3.
fafx: facet-frostex
Strong echinus-like eyes, darkening with age with glistening frosted appearance. Homozygous females sterile, but sterility may be separable from fafx (Kaplan and Hayes, 1967, DIS 42: 38).
fag: facet-glossy
Eyes have facets more irregular than fa, but surface is smoothed, giving a glossy effect. Equal mutant expression in both sexes. Pigment distribution may be uneven, contributing to an impression of altered eye color. No wing effect. Eyes of fag/fa1 intermediate between the two homozygotes. Complementary with spl, fano, nd, and nd2 (Welshons, 1965, Science 150: 1122-29). RK1.
fag58
Large, rough eye with semiglazed surface and irregular pigment distribution causing a patchy red color. About 2/3 flies have incisions of the inner wing margin. Viable and fertile as a male, reduced fertility in females (Fahmy, 1958, DIS 34: 49).
fag62
Like fag and cannot be distinguished from it. In heterozygotes with N mutants and in fag62/fag, the fag phenotype is exhibited; fag62/fa1 has a fa1 phenotype, and fag62/spl is wild type.
*fal: facet-lethal
fal/fa1 resembles fa1/fa1; not notched. Homozygous lethal. RK2.
fal2
A male-lethal allele of Notch. Females nearly wild type but show occasional slight traces of Notch. Full complementation with spl but interacts with fag showing rough irregular eyes.
faswb: facet-strawberry
In males, eyes are rough with a variable tendency to be glossy; with fag and fag62, eyes are very rough, but mutant condition is not as extreme as that found in homozygous glossy-eyed mutants. In heterozygotes with fa1, eyes are slightly rough, overlapping wild type; with spl, the eyes are wild type. The faswb allele, like fa1, is not dosage compensated, and the mutant condition is poorly expressed in females. faswb/fano has slight deltas at junction of longitudinal veins with marginal veins; faswb complements nd and nd2; and in heterozygotes of faswb, N55e11 and N264-40, the eyes are glossy and the Notch phenotype is enhanced, resulting in reduced viability and fertility; with the temperature-sensitive N60g11, heterozygotes are less mutant, viable, and fertile. In double mutants, faswb fag, the males have fag-like eyes; and wing veins are thickened and delta like at tips; they resemble fano males except that wings are seldom notched. The wing-venation effect is less extreme in homozygous females (Welshons and Keppy, 1975, Genetics 80: 143-55; Keppy and Welshons, 1977, Genetics 85: 497-506).
l(1)N: lethal (1) Notch (W.J. Welshons)
There are four phenotypic varieties of l(1)N alleles: (1) Those that are lethal with N and wild type with the recessive visibles [see l(1)N1]; (2) Those that are lethal with N but not wild type with the recessive visibles [see l(1)N2, l(1)N3]; (3) Alleles whose heterozygotes with N+ have a phenotype not recognized as Notch [see l(1)NB], or (4) Alleles that are temperature sensitive for lethality and do not express a Notch phenotype in heterozygotes with N+ [see l(1)Nts]. The embryological defects in l(1)N1 are related to those in N; the development in l(1)NB is sufficiently normal to escape embryonic lethality (Poulson, 1967, 1968).
l(1)N1
l(1)N1/+ females are wild type; l(1)N1/N females and l(1)N1/Y males are lethal; l(1)N/Y;Dp(1;2)51b males are Co-like. Heterozygotes with recessive visibles at Notch are wild type. Developmental defects in l(1)N1/Y males are more limited than in N/Y males and the defects are confined to the anterior ectoderm (Poulson, 1967; 1968). Like N mutants, l(1)N1 mutants are defective as embryos (Shellenbarger and Mohler, 1975, 1978).
l(1)N2
l(1)N2/+ females are wild type; l(1)N2/N females and l(1)N2/Y males are lethal. Heterozygotes with fa and fag are fa-like; with nd, they have nd-like wings and small eyes; with nd3, they are viable, fertile and nd3-like. Developmental defects in l(1)N2/Y males and time of lethal effect same as in l(1)N1/Y. Some l(1)N2/l(1)Nts1 females survive to late pupal stage (Shellenbarger and Mohler, 1975).
l(1)N3
Same as l(1)N2.
l(1)NB
l(1)NB females have small eyes, fewer mesonotal bristles, and, sometimes, bald areas on the thorax (Welshons, 1965). The dominant bristle effect is more extreme in l(1)NB/Y;Dp(1;2)51b males than in l(1)NB/+ females. Heterozygotes with fa have fa-like eyes and, frequently, nicked wings; with nd, they show notched wings and thickened veins; with nd3, they are viable, fertile, and fa-like. l(1)NB/Y males die during early larval life (Poulson, 1967). l(1)NB/l(1)Nts1 females die before pupation (Shellenbarger and Mohler, 1975). Bristle effect autonomous in l(1)NB cells; homozygous mutant cells survive in mosaics (Arnheim, 1967).
l(1)N69e
l(1)N69e/l(1)N69e and l(1)N69e/Df(1)N-8 females are lethal at 18 and 29; l(1)N69e/+ heterozygotes are almost always wild type. l(1)N69e homozygotes die before pupation, but l(1)N69e/l(1)Nts1 heterozygotes survive until the pupal stage.
l(1)Nts1
l(1)Nts1/+ females are wild type at 18 and 29, while l(1)Nts1/Df(1)N-8 females are lethal at 29, but a few escapers are found at 18. l(1)Nts1 homozygotes are viable at 18, but lethal at 29. If homo- and hemizygotes kept at 18C until eclosion are transferred to 29C and kept at this temperature for six days, they gradually become flightless and show gross histological changes in the flight muscles (Vikki and Portin, 1987, William Roux's Arch. Dev. Biol. 196: 12-15). Heterozygotes show recessive visible defects at 18, but not at 29. l(1)Nts1/l(1)N2 and l(1)Nts1/l(1)N3 females survive until the late pupal stage at 29. When heat pulses are given to pupae prior to sensillum-precursor-cell-determination, extra sensilla are produced; when given after sensillum-precursor-cell determination, the precursor cells form neurons only, not accessory cells (Hartenstein and Posakony, 1990, Dev. Biol. 142: 13-30).
l(1)Nts2
Similar to l(1)Nts1 except for occasional survival of homozygotes to the pupal stage at 29 and weaker expression of recessive visible defects in heterozygotes at this temperature.
N: Notch (W.J. Welshons)
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N8
Mohr, 1924, Z. Induktive Abstammungs-Verebungslehre 32: 118.
Mutant alleles are characterized by the following types of expression: Wings of heterozygotes incised at tips and often along edges; veins L3 and L5 thickened; thoracic microchaetae crowded and irregularly distributed (Mohr, 1919, Genetics 4: 275-82; 1923, Z. Indukt. Abstamm. Vererbungsl. 32: 108-232). Males and homozygous females are lethal. In some N mutants, the phenotype is mild and varies in one or more of its typical features, but such N's can usually be identified by phenotypes expressed when heterozygous with recessive visible eye and wing mutants that also occur at Notch. Females N/N+ are Notch; females N/N+;Dp(1;2)51b (representing a duplication for the Notch locus) are wild type. In the hemizygous male, N/Y is lethal, whereas N/Y;Dp(1;2)51b is viable and phenotypically normal; the wild phenotype is dependent upon the presence of the normal dosage of 3C6-7 for each sex. An extra dose of 3C6-7 [as in Dp(1;2)51b or Dp(1;1)Co] causes the expression of the dominant phenotype Confluens (Co); thus N+/N+;Dp(1;2)51b females and N+/Y;Dp(1;2)51b males are Co-like (Welshons, 1965). Deficiency mapping places Co to the left of N (Merriam). Homozygotes and hemizygotes for all N mutants suffer the same embryological defects. In developing embryos, the pattern of differentiation of anterior and ventral embryonic ectoderm is aberrant; both presumptive hypoderm and presumptive neuroblasts develop as neuroblasts, resulting in embryos with a hypertrophied central nervous system lacking ventral and ventral-lateral hypoderm [Poulson, 1939, DIS 12: 64-65; 1940, J. Exp. Zool. 83: 271-325; 1950, Biology of Drosophila (M. Demerec, ed.). Wiley, New York, pp.168-274; 1967, DIS 42: 81; Wright, 1970, Adv. Genet. 15: 305-15]. Sensillum differentiation in peripheral nervous system of embryos also abnormal (Hartenstein and Campos-Ortega, 1986, Roux's Arch. Dev. Biol. 195: 210-21). In mosaic embryos (N/N+ and N/0 cells), the N/0 cells never give rise to hypoderm within the neurogenic region (Hoppe and Greenspan, 1986, Cell 46: 773-83). However, single N/0 cells transplanted to N+ recipient embryos can give rise to hypoderm (Technau and Campos-Ortega, 1987, Proc. Nat. Acad. Sci. USA 84: 4500-04).
N81k10
Typical Notch.
N264-66
Wing-notching weak and rarely visible. N264-66/fa heterozygotes variegate for fa. Some N264-66/Y males are viable and have cream-colored eyes with spots of normal red pigment.
N55e11
A weak Notch. Deltas on wing veins are most reliable character for classification. Lethal when heterozygous with nd3, N60g11, and NCo. In homozygotes and hemizygotes hyperplasia of central nervous system extreme; embryonic peripheral nervous system abnormal with sensilla undifferentiated (Hartenstein and Campos-Ortega, 1986, Wilhelm Roux's Arch. Dev. Biol. 195: 210-21).
N60g11
Wings seldom notched; veins thickened; deltas at tips. N60g11/+ heterozygotes have normal eyes at 29 and a disrupted facet arrangement at 21. With increasing temperature, rough eye phenotype diminishes and Notch mutant characteristics are expressed. TSP for disrupted facets is in the third instar. N60g11/N60g11 Dp(1;2)51b7 females are viable at 29; survival sharply decreased at 20-23; TSP for lethality in middle of embryonic stage. N60g11/fa flies have eyes like fa. Semilethal with nd3. Viability poor with nd.
N64d6
Typical Notch. N64d6 spl flies cannot be distinguished from N64d6 spl+ flies. When spl is coupled to N64d6, spl is not enhanced by E(spl).
N66h26
The Notch inversion N66h26 (synonym: In(1)w8xN66h26), with breakpoints in w and N, was derived from Df(1)N-8 and is unstable in crosses involving a wafagrb stock, giving rise to N+ revertants such as w8x1N+ and w8x2N+ (Welshons and Keppy, 1981; Grimwade et al., 1985). Recombination hetween w and N, which does not occur in N66h26, does take place in these reversions, indicating that reversion to N+ is accompanied by reinversion of In(1)N66h26. The w8x1N+ derivative of N66h26 is also unstable in crosses involving the wafagrb stock, generating (stepwise) various mutant and wildtype Notch alleles (Grimwade et al., 1985). Df(1)w79, another derivative of N66h26, is deficient for both N and w (Welshons and Keppy, 1981).
N68j
Typical Notch. N68j/+ females have wings excised at the tips; N68j/spl females are spl. N64j flies carrying Dp(1;1)Co are almost wild type. Mutant males with w+Y are viable (Hayman and Maddern, 1969).
N68j1
Typical Notch. N68j1/Df(1)N-8 females are lethal at 29 and 18; Notch-wing phenotype shows little or no response to temperature (Shellenbarger and Mohler, 1975).
N69c
Shows variable Notch-wing expression depending on temperature. Lethal in homozygotes and in heterozygotes with Df(1)N-8 at 29 and 18. N69c/+ heterozygotes show greater expression of Notch-wing at 18 than at 29 (Shellenbarger and Mohler, 1975).
N76b8
Typical Notch.
N77c17
Typical Notch.
N80j9
Typical Notch. Genetically unstable, giving rise spontaneously to six independent N+ revertants. The N+10 revertant is rather unstable (Grimwade et al., 1985).
N81k3
Typical Notch.
N81k6
Typical Notch.
N81k8
Typical Notch.
N81k9
Typical Notch.
N81l1
Typical Notch.
N81l3
Typical Notch.
N81l5
Typical Notch.
N81l9
Typical Notch.
N264-40
Typical Notch. Male embryos show developmental abnormalities like those of Df(1)N-8 (Poulson, 1939). Lethal with nd3.
N264-47
Typical Notch. Male embryos show developmental abnormalities like those of Df(1)N-8 (Poulson, 1939). Lethal with nd3.
N264-103
Temperature-sensitive Notch allele. N264-103/nd3 females are viable at 22o and lethal at 29o, with a long, possibly polyphasic, TSP beginning in the embryonic stage. N264-103/spl females show eye-facet disarray, notching, bristle-number variation, and tarsal-segment fusion, the TSP being in the third instar (Foster, 1973). N264-103/spl variegates for spl; N264-103/fa is fa.
N264-107
Typical Notch.
N264-109
Typical Notch except for semilethality with nd3.
NCo
Wing tips seldom notched; veins thickened, with deltas. Acrostichal rows irregular. NCo/nd3 heterozygotes lethal; rare survivors sterile and weak. NCo/+ females show thickened wing veins (a Confluens-like phenotype) more frequently than nicked or notched wings. Also, NCo heterozygous females with an extra dose of 3C6-7 [Dp(1;1)Co or Dp(1;2)51b] or hemizygous males with Dp(1;2)51b have an enhanced Confluens-like wing phenotype.
NhdA171
Typical Notch.
NhdC8
Typical Notch.
Nj24
Typical Notch. Lethal with nd3.
NM: Notch Mischiakow
Wings notched at tips and occasionally at sides; veins thickened, with deltas. Eyes slightly smaller than normal; occasionally one eye extremely small.
NNic: Notch Nicoletti
Typical Notch. Lethal with nd3. Cell lethal in tergites and dorsal mesothorax (Ripoll and Garcia-Bellido, 1979, Genetics 91: 443-53).
NS: Notch Schalet
Weak Notch. NS/AxS is lethal.
nd: notchoid (W.J. Welshons)
Wings notched and veins thickened. The notching is found mostly on anterior and posterior margins and is the result of cell death (Thompson and Spivey, 1984, Genet. Res. 44: 201-69). Homozygotes are viable and fertile in both sexes. N/nd1 heterozygotes are partially viable and relatively infertile (Portin, 1977) and show notched and straplike wings and small eyes. About 10% of fa/nd1 flies have small notches in one or both wings. nd3/nd1 heterozygotes have slightly thickened wing veins with deltas; spl/nd1 heterozygotes lack a few bristles (like spl/+) and their eyes are sometimes smaller than normal and roughened. spl nd1 males have rough eyes, nd-like wings, and irregular, bushy sex combs.
nd0
thumb
nd0 (= fan)
From Glass, 1933, J. Genet. 27: 233-41.
Wings have apical nicks or notches in 90-100% of males, but only 8% of homozygous females. Eyes not rough. fa/nd0 is wild type. Viability and fertility excellent. RK2 in male.
nd1
nd1 is temperature-sensitive. In homozygotes at 29, the eyes are rough and reduced in size, there is extreme wing notching, and wing veins are thick; at 25, the abnormalities are less severe, and at 18, the eyes are normal and the wings are nicked. At 29, heterozygotes with fa, fag, and spl are complementary (Foster, 1973; Shellenbarger and Mohler, 1975). nd1/Y;E(spl)r19/+ males have severely reduced and crumpled wings (Xu, Rebay, Fleming, Scottgale, and Artavanis-Tsakonas). Wing development also affected in nd1/Y;mam10/+ males. nd1 and mam10 double heterozygotes are wild type. Wing notching is suppressed in nd1/Y males by Dl/+.
nd2
nd2/nd2 and nd2/nd1 flies resemble nd1 homozygotes; nd2/nd3 heterozygotes are noncomplementary (Welshons). The nd2 allele is temperature sensitive; in homozygotes at 29, the eyes are small and rough (spl-like), wings have extreme notches, wing veins are thickened, tarsi are shortened, and the mutants are semilethal as late pupae; at 25, the abnormalities are much less severe; at 18, the eyes are slightly spl-like, wings are nicked, wing veins are incomplete, some bristles are missing, and the mutants are semilethal as late pupae. At 29, fa/nd2 heterozygotes have nicked wings, spl/nd2 heterozygotes are spl-like, and nd4/nd2 heterozygotes resemble N/+ (Shellenbarger and Mohler, 1975). Similar wing abnormalities in nd1/Y;E(spl)r19/+ and nd2/Y;E(spl)r19/+ males. The temperature-sensitive rough-eye phenotype of nd2 is enhanced by E(spl)/+ (Xu et al.).
nd3
Wings of both sexes notched at ends of L3 and L4 veins; wing veins enlarged and delta-like at tips. Mild mutant expression often limited to wing-vein effect. Mutant expression diminished at high temperature (Shellenbarger and Mohler, 1975, Genetics 81: 143-62). Heterozygotes show extremely weak dominance. nd3/N almost completely lethal; survivors are sterile and have an exaggerated Notch phenotype. nd3/fa closely resembles wild type. Heterozygotes with fag and spl are complementary; with nd and nd2, heterozygotes are noncomplementary with a mild mutant expression of nd3-like wings. Up to 5% of nd3 males from aged cultures show hyper- and hypodeveloped external genitalia (Kroeger, 1960, J. Morphol. 107: 227-32).
nd3.1072
Viable when homo- or hemizygous; shows adult wing nicking. Lethal when heterozygous with N deficiencies. Phenotype similar to nd.
nd3.1072rv
Wild-type revertant of nd3.1072. Viable in combination with N deficiencies.
nd4
Temperature sensitive and semilethal in homozygotes; wing phenotype more extreme and survival greater at 18 than at 29. nd4/+ lethal at both temperatures.
ndts69d
Like ndts69j (see below).
ndts69f
Like ndts69j (see below).
ndts69j
Temperature-sensitive semilethal. Homozygotes express weak notches, mild deltas, and extra bristles at both 18 and 29; both homozygotes and hemizygotes show significantly better survival at 18 than at 29. ndts69j/+ heterozygotes have normal wings at 18 and 29. Df(1)N-8/ndts69j heterozygotes have significantly better survival at 18 than at 29.
ndts70j
In general, ndts70j homozygotes and heterozygotes resemble the other Nts mutants. ndts70j homozygotes, however, are wild type at 18 and some ndts70j/+ heterozygotes have notched wings at 29.
spl (W.J. Welshons)
In homozygotes, eyes are rough and small, bristles are often doubled or split (sometimes missing). Hemizygotes show a more extreme reduction in eye size as well as an increase in facet and bristle abnormalities (Shephard et al., 1989). Both eye and bristle abnormalities occur at all temperatures from 18 to 29, an exception being a spl stock from Novosibirsk, Russia, that shows temperature sensitivity (Mglinetz, 1980, DIS 55: 107-08). The bristle phenotype is caused by an extra division of an initial bristle-forming cell (Lees and Waddington, 1943, Proc. R. Soc. London, B 131: 87-110; Van Breugel and Van der Aart, 1979, Dev. Biol. 186: 267-71). A few bristles (sockets remaining) are usually removed from the posterior border of tergites in spl/+ heterozygotes (Welshons). The eye abnormalities are the result of abnormal differentiation of photoreceptors at the morphogenetic furrow (Cagan and Ready, 1989). Heterozygotes with the other recessive visibles at Notch are almost normal except for spl/nd2 flies; the latter are spl-like at 29 (Shellenbarger and Mohler, l975). Another temperature-sensitive effect is shown by N264-103/spl flies, which have abnormal eye facets at 28-29 but are almost wild type at 20-22 (Foster, 1973, Dev. Biol. 32: 282-96). The spl phenotype can be enhanced by E(spl)/+ or E(spl)/E(spl). spl/+;E(spl)/+ flies resemble spl/spl flies; spl/spl; E(spl)/+ and spl/Y; E(spl)/+ flies show a very extreme mutant phenotype (Shephard et al., 1989). spl/Y;E(spl)R19/+ males and spl/+;E(spl)R19/+ females show spl and Ax-like phenotypes (Xu et al.). The spl phenotype is reduced in mam heterozygotes. When, however, spl is coupled to a N point mutant, as in N64d6 spl/+ +;E(spl)/+, the phenotype is not spl (Welshons, 1971) split behaves autonomously in mosaics in regard to both eye and bristle phenotypes (Stern and Tokunaga, 1968, Proc. Nat. Acad. Sci. USA 60: 1252-59). The spl phenotype becomes dominant if spl is coupled, in cis, to lethal Ax alleles. Thus Ax spl/++ is spl, while +spl/++ is wild type (Welshons, 1971; Kelley et al., 1987).
*spl2
Resembles spl except for smaller eyes.
Summary (Interactive Fly)

transmembrane receptor - neurogenic - responsible for lateral inhibition and cell fate choices

Gene Model and Products
Number of Transcripts
2
Number of Unique Polypeptides
1

Please see the JBrowse view of Dmel\N for information on other features

To submit a correction to a gene model please use the Contact FlyBase form

Protein Domains (via Pfam)
Isoform displayed:
Pfam protein domains
InterPro name
classification
start
end
Protein Domains (via SMART)
Isoform displayed:
SMART protein domains
InterPro name
classification
start
end
Structure
Protein 3D structure   (Predicted by AlphaFold)   (AlphaFold entry P07207)

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Model Confidence:
  • Very high (pLDDT > 90)
  • Confident (90 > pLDDT > 70)
  • Low (70 > pLDDT > 50)
  • Very low (pLDDT < 50)

AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.

Experimentally Determined Structures
Crossreferences
PDB - An information portal to biological macromolecular structures
Comments on Gene Model

Low-frequency RNA-Seq exon junction(s) not annotated.

Gene model reviewed during 5.52

Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0070507
10150
2703
FBtr0304659
9611
2703
Additional Transcript Data and Comments
Reported size (kB)

10.2 (unknown)

10.4 (sequence analysis)

11.7 (northern blot)

Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
UniProt
RefSeq ID
GenBank
FBpp0070483
288.9
2703
5.04
FBpp0293201
288.9
2703
5.04
Polypeptides with Identical Sequences

The group(s) of polypeptides indicated below share identical sequence to each other.

2703 aa isoforms: N-PA, N-PB
Additional Polypeptide Data and Comments
Reported size (kDa)
Comments
External Data
Subunit Structure (UniProtKB)

Homomer. Interacts with Su(H) when activated. Interacts with Dx via its ANK repeats. Interacts with Delta via the EGF repeats and the Delta EGF repeats. Interacts with Nedd4 and Su(dx). Interacts with O-fut1; the interaction glycosylates N and transports N to early endosomes. Interacts with Akap200; the interaction stabilizes N/Notch protein levels by preventing Cbl-mediated ubiquitination and subsequent lysosomal degradation of N/Notch (PubMed:29309414).

(UniProt, P07207)
Post Translational Modification

Upon binding its ligands such as Delta or Serrate, it is cleaved (S2 cleavage) in its extracellular domain, close to the transmembrane domain. S2 cleavage is probably mediated by Kuz. It is then cleaved (S3 cleavage) downstream of its transmembrane domain, releasing it from the cell membrane. S3 cleavage requires Psn.

O-glycosylated (PubMed:27268051). Three forms of O-glycosylation (O-fucosylation, O-glucosylation and O-GlcNAcylation) are detected (PubMed:27268051). O-fucosylated by O-fut1 and fng in the EGF repeat domain inhibits both Serrate/Ser- and Delta/Dl-binding (PubMed:10935637, PubMed:12909620). O-glucosylation by rumi in the endoplasmic reticulum is necessary for correct folding and signaling (PubMed:18243100).

Ubiquitinated by various ubiquitin ligases; which promotes ligand-independent endocytosis and proteasomal degradation (PubMed:15620649, PubMed:22162134). Ubiquitinated by Nedd4 (PubMed:15620649). May also be ubiquitinated by Su(dx) and Cbl (PubMed:29309414). Mono-ubiquitinated, possibly by dx/deltex; this may be involved in the ESCRT-III mediated targeting to multivesicular bodies (PubMed:22162134).

(UniProt, P07207)
Domain

Crystal structure of the ANK repeat domain shows that there are 7 repeats and the stabilizing C-terminal repeat enhances the protein stability by extending the ankyrin domain.

(UniProt, P07207)
Linkouts
Sequences Consistent with the Gene Model
Nucleotide / Polypeptide Records
 
Mapped Features

Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\N using the Feature Mapper tool.

External Data
Crossreferences
Linkouts
Expression Data
Testis-specificity index

The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).

-0.50

Transcript Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
northern blot
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data

Expression of the N transcript is ubiquitous until later embryonic stages, where expression is first resticted to the ectoderm and mesoderm, and finally only detected ventrally along the periphery of the central nervous system.

By northern blot analysis, the largest N transcript is expressed at high levels during embryogenesis, pupal stages and in the adult.

Additional N transcripts, ranging in size fro, 0.7 kb to 4.5 kb, are expressed at high levels during various stages of development.

The major N transcript is detected at high levels in 4-5 hour and 9-12 hour old embryos, and with longer autoradiograph exposures it is detected in all embryonic stages, in larvae, pupae and adults. N transcript is detected in 7 day old pupae, but not in 8 day old pupae. The N transcript expression pattern corrolates with the requirement of N activity for survival.

N transcript expression is highest in stage 10-13 embryos. Longer exposures of the autoradiograms show expression in the late embryo, low levels in the larvae and expression is detected in pupae and adults.

The N transcript is expressed throughout development, with the highest levels reached during embryogenesis.

Marker for
 
Subcellular Localization
CV Term
Polypeptide Expression
immunolocalization
Stage
Tissue/Position (including subcellular localization)
Reference
mass spectroscopy
Stage
Tissue/Position (including subcellular localization)
Reference
western blot
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data

Notch activity is moderately high and ubiquitous in all cells of the lymph gland lobes, with crystal cells exhibiting the highest levels.

In stage 16, expression of Dl in the ventral side of the ileum activates the N receptor in neighboring dorsal ileum cells, inducing their diferentiation into two rows of hindgut boundary cells.

N protein is observed throughout the late larval and early pupal wing disc. Levels are elevated at the anterior posterior (AP) and dorsal ventral (DV) border regions.

N protein is strongly expressed in neuroepithelial cells of the inner and outer optic anlagen (IPC, OPC) from late second to late third instar larval stages. N expression is downregulated in the medial cells in the OPC that become medulla neuroblasts. N protein is strongly expressed in medulla neurons and their axons, in the medulla neuropil, and in the lamina.

In region 3 of the germarium, N can be seen in all follicle cells, but is more expressed in polar and stalk cell precursors.

N protein is expressed in the invaginating ectodermal cells of the keyhole structure of the developing embryonic proventriculus. N protein is upregulated in the anterior- and posterior-most cell rows of the keyhole structure after embryonic stage 15.

N protein is expressed ubiquitously at the cell membrane of all cells of the visceral mesoderm. Expression appears to be lower in the bap-expressing fusion-competent myoblasts.

Protein is detected ubiquitously in third instar larval leg discs. At 34-38 hours after pupal formation N protein is expressed in the leg joints in the distal joint tissue apodemes.

N-protein is detected in each adult tagma via Western Blot analysis directly after eclosion. Expression in head and thorax persists until 20 days post eclosion while the amount of N-protein in the adult abdomen declines.

N protein and Dl protein localization were compared during oogenesis. In the germarium, cytoplasmic N and Dl protein staining are observed. In contrast to Dl protein, more intense N staining is seen in the membranes of follicle cells in regions 2 and 3 of the germarium. Diffuse cytoplasmic staining of N and Dl proteins is observed in stages 1-6. In contrast to Dl protein, follicle cell membrane staining of N protein is observed during this whole period. In stages 4-5, N and Dl protein accumulation is apically polarized within the membranes of all follicle cells but some N protein is also present in the basal membranes. N and Dl protein staining is also observed in nurse cell membranes and cytoplasm but the membrane staining is stronger for Dl protein than N protein. By stages 7-8, in contrast to Dl protein, N protein is still present in the membranes between oocytes and follicle cells. N protein is expressed in the membranes of all follicle cells that surround the egg chamber in stages 7-9. From stage 9, N protein accumulation decreases in follicle cell membranes but persists in nurse cell membranes. N protein also accumulates in two specialized groups of follicle cells situated dorsolaterally at the nurse cell chamber-oocyte junction which eventually form the chorionic appendages. No Dl accumulation is seen in these cells. While Dl protein appears to be transferred from nurse cells to the oocyte during stage 11, N protein is not transferred.

Marker for
Subcellular Localization
CV Term
Evidence
References
inferred from mutant phenotype
inferred from mutant phenotype
located_in cell surface
inferred from direct assay
colocalizes_with cytoplasmic vesicle
inferred from direct assay
located_in cytoplasm
inferred from direct assay
located_in early endosome
inferred from direct assay
inferred from direct assay
inferred from mutant phenotype
located_in endosome
inferred from direct assay
colocalizes_with late endosome
inferred from direct assay
located_in late endosome
inferred from direct assay
colocalizes_with lysosome
inferred from direct assay
located_in membrane
inferred from direct assay
located_in nucleus
inferred from mutant phenotype
inferred from physical interaction with FLYBASE:Su(H); FB:FBgn0004837
Expression Deduced from Reporters
Reporter: P{hs-N+-GV}
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
High-Throughput Expression Data
Associated Tools

JBrowse - Visual display of RNA-Seq signals

View Dmel\N in JBrowse
RNA-Seq by Region - Search RNA-Seq expression levels by exon or genomic region
Reference
See Gelbart and Emmert, 2013 for analysis details and data files for all genes.
Developmental Proteome: Life Cycle
Developmental Proteome: Embryogenesis
External Data and Images
Linkouts
BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
DRscDB - A single-cell RNA-seq resource for data mining and data comparison across species
EMBL-EBI Single Cell Expression Atlas - Single cell expression across species
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
FlyAtlas2 - A Drosophila melanogaster expression atlas with RNA-Seq, miRNA-Seq and sex-specific data
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
Images
Alleles, Insertions, Transgenic Constructs, and Aberrations
Classical and Insertion Alleles ( 390 )
For All Classical and Insertion Alleles Show
 
Other relevant insertions
Transgenic Constructs ( 320 )
For All Alleles Carried on Transgenic Constructs Show
Transgenic constructs containing/affecting coding region of N
Transgenic constructs containing regulatory region of N
Aberrations (Deficiencies and Duplications) ( 180 )
Inferred from experimentation ( 180 )
Gene disrupted in
Gene not disrupted in
Inferred from location ( 22 )
Variants
Variant Molecular Consequences
Alleles Representing Disease-Implicated Variants
Phenotypes
For more details about a specific phenotype click on the relevant allele symbol.
Lethality
Allele
Sterility
Allele
Other Phenotypes
Allele
Phenotype manifest in
Allele
adult thorax & microchaeta
adult thorax & microchaeta, with Scer\GAL4pnr-MD237
adult thorax & microchaeta (with Nl1N-ts1)
adult thorax & microchaeta (with NMcd1)
adult thorax & microchaeta (with NMcd5)
adult thorax & microchaeta (with NMcd8)
adult thorax & microchaeta | somatic clone
chemosensory sensory organ & wing vein L1 & glial cell, with Scer\GAL4hs.PB
chemosensory sensory organ & wing vein L1 & glial cell | supernumerary
chemosensory sensory organ & wing vein L3 & glial cell, with Scer\GAL4hs.PB
chemosensory sensory organ & wing vein L3 & glial cell | supernumerary
chordotonal organ precursor cell & ventral thoracic disc, with Scer\GAL4sca-109-68
cuticle & macrochaeta | somatic clone
dorsal mesothoracic disc & filamentous actin | conditional ts
dorsal mesothoracic disc & filamentous actin | somatic clone, with Scer\GAL4Act5C.PI
dorsal mesothoracic disc & sensory mother cell
dorsal pouch & epidermis
embryonic/larval dorsal branch & tracheal tip cell
embryonic/larval dorsal branch & tracheal tip cell, with Scer\GAL4btl.PS
embryonic/larval trachea & tracheal tip cell, with Scer\GAL4btl.PS
embryonic hypopharynx & epidermis
embryonic labial segment & embryonic epidermis
embryonic labral segment & embryonic epidermis
embryonic maxillary segment & embryonic epidermis
external sensory organ precursor cell IIb & mechanosensory sensory organ | conditional ts
eye & neuron | somatic clone
eye disc & neuron | somatic clone
eye photoreceptor cell & eye disc | conditional ts
fascicle & antennal segment 3, with Scer\GAL4sca-P309
fascicle & antennal segment 3 | conditional ts
follicle cell & nucleus | somatic clone
fusion competent cell & visceral mesoderm
glial cell & antennal segment 3 | ectopic, with Scer\GAL4sca-P309
glial cell & antennal segment 3 | ectopic | conditional ts
labellum & macrochaeta
leg & joint, with Scer\GAL4dpp.blk1
leg & joint, with Scer\GAL4klu-G410
macrochaeta & head | conditional ts
macrochaeta & mesothoracic tergum, with Scer\GAL4sca-109-68
macrochaeta & postnotum, with Scer\GAL4ptc-559.1
macrochaeta & pronotum
macrochaeta & scutum
macrochaeta & scutum | conditional ts
macrochaeta & scutum | somatic clone
macrochaeta & thorax
macrochaeta & thorax | anterior | dorsal | somatic clone
macrochaeta & wing
mechanosensory sensory organ & wing vein L1 & glial cell, with Scer\GAL4hs.PB
mechanosensory sensory organ & wing vein L1 & glial cell | supernumerary
mechanosensory sensory organ & wing vein L3 & glial cell, with Scer\GAL4hs.PB
mechanosensory sensory organ & wing vein L3 & glial cell | supernumerary
mesothoracic tergum & macrochaeta, with Scer\GAL4sca-C253
microchaeta & antennal segment 3, with Scer\GAL4sca-P309
microchaeta & antennal segment 3 | conditional ts
microchaeta & head | conditional ts
microchaeta & scutum
microchaeta & scutum | conditional ts
microtubule & oocyte
mitotic cell cycle & eye disc | conditional ts
muscle founder cell & visceral mesoderm
neuroblast & larval brain
neuroblast | supernumerary & larval brain | somatic clone, with Scer\GAL4Act5C.PI
ommatidium & eye disc | male
photoreceptor cell & eye disc | male
photoreceptor cell R8 & eye disc | male
procephalic segment & epidermis
proneural cluster & dorsal mesothoracic disc
proneural cluster & dorsal mesothoracic disc, with Scer\GAL4ptc-559.1
scutum & macrochaeta
scutum & macrochaeta | ectopic (with Df(1)N-8)
scutum & microchaeta
scutum & microchaeta & tormogen cell | conditional ts
scutum & microchaeta & trichogen cell | conditional ts
sensory mother cell & dorsal mesothoracic disc
sensory mother cell & dorsal mesothoracic disc, with Scer\GAL4sd-SG29.1
socket & scutum | somatic clone
tarsal segment 4 & joint, with Scer\GAL4ap-md544
tarsal segment 4 & joint | ectopic
thorax & macrochaeta
thorax & microchaeta
thorax | dorsal & macrochaeta, with Scer\GAL4pnr-MD237
tormogen cell & antennal segment 3 | conditional ts, with Scer\GAL4sca-P309
tormogen cell & antennal segment 3 | ectopic | conditional ts, with Scer\GAL4sca-P309
tormogen cell & mesothoracic tergum | supernumerary, with Scer\GAL4sca-109-68
trichogen cell & antennal segment 3 | conditional ts, with Scer\GAL4sca-P309
trichogen cell & antennal segment 3 | ectopic | conditional ts, with Scer\GAL4sca-P309
wing (with N1)
wing (with Nopa23)
wing & macrochaeta
wing & macrochaeta, with Scer\GAL4sd-SG29.1
wing & microchaeta, with Scer\GAL4ptc-559.1
wing vein L1 & wing nerve
Orthologs
Human Orthologs (via DIOPT v9.1)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
Homo sapiens (Human) (111)
11 of 14
Yes
Yes
10 of 14
No
Yes
9 of 14
No
Yes
5 of 14
No
Yes
4 of 14
No
No
1  
3 of 14
No
No
6  
3 of 14
No
Yes
3 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
1  
2 of 14
No
No
0  
2 of 14
No
No
2  
2 of 14
No
No
2 of 14
No
No
0  
2 of 14
No
No
2 of 14
No
Yes
1  
2 of 14
No
Yes
2  
2 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
2  
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
2  
1 of 14
No
No
1  
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
2  
1 of 14
No
No
6  
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1  
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
2  
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1  
1 of 14
No
Yes
Model Organism Orthologs (via DIOPT v9.1)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
Rattus norvegicus (Norway rat) (72)
13 of 14
Yes
Yes
12 of 14
No
Yes
9 of 14
No
Yes
5 of 14
No
Yes
3 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
Mus musculus (laboratory mouse) (78)
12 of 14
Yes
Yes
0  
12 of 14
Yes
Yes
9 of 14
No
Yes
5 of 14
No
Yes
4 of 14
No
No
3 of 14
No
No
3 of 14
No
No
3 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
Xenopus tropicalis (Western clawed frog) (71)
10 of 13
Yes
Yes
9 of 13
No
Yes
6 of 13
No
Yes
6 of 13
No
No
3 of 13
No
Yes
2 of 13
No
No
2 of 13
No
No
2 of 13
No
No
2 of 13
No
Yes
2 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
No
1 of 13
No
No
1 of 13
No
No
1 of 13
No
Yes
1 of 13
No
No
Danio rerio (Zebrafish) (97)
12 of 14
Yes
Yes
11 of 14
No
Yes
10 of 14
No
Yes
10 of 14
No
Yes
4 of 14
No
No
3 of 14
No
No
3 of 14
No
Yes
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
2 of 14
No
Yes
2 of 14
No
No
2 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
Caenorhabditis elegans (Nematode, roundworm) (50)
9 of 14
Yes
Yes
7 of 14
No
Yes
6 of 14
No
No
3 of 14
No
No
2 of 14
No
No
2 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
Yes
1 of 14
No
No
1 of 14
No
No
1 of 14
No
Yes
1 of 14
No
No
Anopheles gambiae (African malaria mosquito) (41)
11 of 12
Yes
Yes
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
1 of 12
No
No
Arabidopsis thaliana (thale-cress) (1)
1 of 13
Yes
No
Saccharomyces cerevisiae (Brewer's yeast) (5)
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
1 of 13
Yes
No
Schizosaccharomyces pombe (Fission yeast) (0)
Escherichia coli (enterobacterium) (2)
1 of 11
Yes
No
1 of 11
Yes
No
Other Organism Orthologs (via OrthoDB)
Data provided directly from OrthoDB:N. Refer to their site for version information.
Paralogs
Paralogs (via DIOPT v9.1)
Drosophila melanogaster (Fruit fly) (40)
5 of 13
3 of 13
3 of 13
3 of 13
3 of 13
2 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
1 of 13
Human Disease Associations
FlyBase Human Disease Model Reports
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 13 )
Allele
Disease
Evidence
References
Potential Models Based on Orthology ( 9 )
Modifiers Based on Experimental Evidence ( 22 )
Allele
Disease
Interaction
References
is exacerbated by CatHMS00990
is ameliorated by CatUAS.cUa
is ameliorated by Sod2UAS.cMa
is exacerbated by cncHMS00650
is exacerbated by Sod2HMS00499
is ameliorated by cncUAS.cSa
ameliorates  carcinoma
Disease Associations of Human Orthologs (via DIOPT v9.1 and OMIM)
Note that ortholog calls supported by only 1 or 2 algorithms (DIOPT score < 3) are not shown.
Homo sapiens (Human)
Gene name
Score
OMIM
OMIM Phenotype
DO term
Complementation?
Transgene?
Functional Complementation Data
Functional complementation data is computed by FlyBase using a combination of the orthology data obtained from DIOPT and OrthoDB and the allele-level genetic interaction data curated from the literature.
Interactions
Summary of Physical Interactions
Interaction Browsers

Please see the Physical Interaction reports below for full details
protein-protein
Physical Interaction
Assay
References
RNA-protein
Physical Interaction
Assay
References
Summary of Genetic Interactions
Interaction Browsers

Please look at the allele data for full details of the genetic interactions
Starting gene(s)
Interaction type
Interacting gene(s)
Reference
suppressible
suppressible
enhanceable
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
enhanceable
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
enhanceable
suppressible
Starting gene(s)
Interaction type
Interacting gene(s)
Reference
enhanceable
enhanceable
suppressible
suppressible
suppressible
suppressible
enhanceable
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
suppressible
enhanceable
suppressible
External Data
Subunit Structure (UniProtKB)
Homomer. Interacts with Su(H) when activated. Interacts with Dx via its ANK repeats. Interacts with Delta via the EGF repeats and the Delta EGF repeats. Interacts with Nedd4 and Su(dx). Interacts with O-fut1; the interaction glycosylates N and transports N to early endosomes. Interacts with Akap200; the interaction stabilizes N/Notch protein levels by preventing Cbl-mediated ubiquitination and subsequent lysosomal degradation of N/Notch (PubMed:29309414).
(UniProt, P07207 )
Linkouts
BioGRID - A database of protein and genetic interactions.
DroID - A comprehensive database of gene and protein interactions.
MIST (genetic) - An integrated Molecular Interaction Database
MIST (protein-protein) - An integrated Molecular Interaction Database
Pathways
Signaling Pathways (FlyBase)
Metabolic Pathways
FlyBase
External Links
External Data
Linkouts
KEGG Pathways - A collection of manually drawn pathway maps representing knowledge of molecular interaction, reaction and relation networks.
SignaLink - A signaling pathway resource with multi-layered regulatory networks.
Class of Gene
Genomic Location and Detailed Mapping Data
Chromosome (arm)
X
Recombination map
1-2
Cytogenetic map
Sequence location
FlyBase Computed Cytological Location
Cytogenetic map
Evidence for location
3C7-3C9
Limits computationally determined from genome sequence between P{EP}EP1362 and P{EP}dncEP1395
Experimentally Determined Cytological Location
Cytogenetic map
Notes
References
3C7-3C8
(determined by in situ hybridisation)
3C7-3C7
(determined by in situ hybridisation)
3C6-3C8
(determined by in situ hybridisation)
3C5-3C11
(determined by in situ hybridisation)
Deficiency mapping places 'Co' to the left of 'N' (Merriam).
There is a discrepancy between the in situ localisation (2C7--2C8) and the molecular localisation based on the flanking sequence (3C7) for the "l(1)G0015" (NG0015) line. The available data suggests that it is most likely that the molecular localisation (3C7) is correct and that the in situs were misinterpreted.
Experimentally Determined Recombination Data
Location
Notes

Nl1N-ts1 maps 0.0018 units to the right of Nspl-1 and to the left of N60g11. Nnd-3 maps 0.06 units to the left of Nspl-1. Nl1N-ts2 maps 0.011 units to the right of Nspl-1. NAx-tsl maps 0.013 units to the right of Nspl-1. Nnd-ts70j maps 0.037 units to the right of Nspl-1 (at the extreme right boundary of the N locus).

Nfa-g maps 0.061 units to the right of N55e11, based on 25/41,200 recombinants. Nnd-3 maps 0.014 units to the right of Nfa-g, based on 8/57,600 recombinants. Nfa-1 maps 0.030 units to the right of N55e11, based on 24/81,000 recombinants. Nfa-1 maps 0.031 units to the left of Nnd-3, based on 8/26,000 recombinants. No recombinants were obtained between Nfa-1 and Nfa-g, out of 65,400 tested chromosomes. N55e11 maps 0.084 units from N264-40, based on 33/78,900 recombinants. N55e11 maps 0.169 units from NCo, based on 37/43,700 recombinants. N55e11 maps 0.180 units from N60g11, based on 41/45,500 recombinants.

N77c17 does not recombine with N60g11 (Welshons).

Stocks and Reagents
Stocks (169)
Genomic Clones (18)
 

Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete

cDNA Clones (64)
 

Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see JBrowse for alignment of the cDNAs and ESTs to the gene model.

cDNA clones, fully sequenced
BDGP DGC clones
Other clones
    Drosophila Genomics Resource Center cDNA clones

    For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.

    cDNA Clones, End Sequenced (ESTs)
    RNAi and Array Information
    Linkouts
    DRSC - Results frm RNAi screens
    Antibody Information
    Laboratory Generated Antibodies
    Commercially Available Antibodies
     
    Developmental Studies Hybridoma Bank - Monoclonal antibodies for use in research
    Cell Line Information
    Publicly Available Cell Lines
    Other Stable Cell Lines
     
    • New stable cell line derived from Kc167 : A stable Kc167 cell line was created to be a "Notch reporter". It contains 24 MS2 stem loops and the coding sequence of LacZ in the endogenous N-regulated E(spl)mbeta-HLH gene in the context of a stable cell line expressing MCP-GFP (MCP-GFP is a MS2-binding protein).

    • New stable cell line derived from S2R+ : A N-expressing stable S2R+ cell line was created.

    • New stable cell line derived from S2-Mt-N : S2 cells stably transformed to express wild-type N from a Cu-inducible metallothionein promoter.

    • New stable cell line derived from S2-unspecified : An S2 cell line stably expressing pMT-N (full-length N under the control of the MtnA promoter) was created.

    • New stable cell line derived from S2-unspecified : S2 cells stably expressing N tagged with EGFP or Ser tagged with tdTomato were used.

    Other Comments

    A Ser-N-cno complex mediates essential interactions between glia and neuroepithelial cells in optic lobe development.

    Haploinsufficient locus (not associated with strong haplolethality or haplosterility).

    N signaling is important for the formation and maintenance of the germline stem cell niche in the ovary.

    There appears to be competition (involving N-mediated lateral inhibition) between tracheal cells during branching morphogenesis, such that those with the highest btl activity take the lead position at the branch tip and those with less btl activity assume subsidiary positions and form the branch stalk.

    The N product prevents br expression in egg chambers.

    N does not promote growth in the eye by acting via ey or toy, but by acting via eyg.

    N signalling contributes to long term memory formation in the adult brain.

    The accumulation of N protein in the late endosome appears to be required for dx-mediated Su(H)-independent N signaling.

    N plays a critical role in mesoderm subdivision prior to its well-established role in lateral inhibition. It does this, at least in part, by modulating levels of twi expression across segments.

    The N/Abl interaction may promote the turning of ISNb axons by attenuating Abl-dependant adhesion of ISNb axons to their substratum, thus releasing the axons to respond to attraction from target muscles.

    N has a role in topologically linking the position of wing veins to prepattern gene expression.

    Myogenic cell fates are antagonised by N only in asymmetric lineages of the heart, with or without cell division.

    l(2)gl acts together with numb in N inhibition and cell fate specification in the adult sensory organ precursor lineage.

    N does not control specific eye field identity by promoting ey expression but it influences eye primordium formation through its control of proliferation.

    dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.

    Glycosylation of the N protein domain 'EGF12' is necessary for fng to inhibit the activation of N signalling by Ser but is not necessary for Ser binding to N.

    Dl signalling, through N, induces the anterior polar follicle cells of the egg chamber to signal through the JAK/STAT pathway and induce the formation of the interfollicle cell (or stalk) between adjacent egg chambers. This stalk formation is necessary for polarization of adjacent younger egg chambers by inducing shape change and preferential adhesion that positions the oocyte at the posterior.

    N is necessary and sufficient for crystal cell specification. It is also required for production of normal levels of lamellocytes following infection of larvae by the parasitic wasp L.boulardi.

    N signalling plays a pivotal role in determining cell fates along the dorsal ventral axis of the hindgut.

    The majority of N protein in Drosophila appears to be full-length. The majority of N protein on the cell surface is full-length and in vivo, furin cleavage of N is not required for its biological activity.

    N is required for gcm expression and glial fate in the dorsal bipolar dendritic (dbd) sensory lineage in the embryonic nervous system.

    Egfr and N signalling pathways act antagonistically in mesothoracic bristle patterning.

    Interacts genetically with 'eyeful' mutant though it is not yet clear whether 'eyeful' corresponds to lola or psq.

    fng plays a key role in positioning N activation during early oogenesis.

    msi is epistatic to N during the asymmetric cell division giving rise to external sensory organ precursor IIa and IIb cells.

    N signalling does not affect msi expression, though msi can act downstream of N, therefore N signalling is more likely to regulate msi activity than its expression.

    The endogenous N gene is rearranged in S2 cells.

    Secreted sca protein associates with and stabilizes N at the cell surface, acting to regulate N activity to sharpen proneural cluster boundaries and ensure establishment of single pioneer neurons.

    N is required for the genesis of a subset of glial cells in the CNS.

    N signalling positively regulates gcm expression in the context of subperineurial glial cell development.

    N acts as a genetic switch between neuronal and glial fates by negatively regulating gcm. N represses neurogenesis or gliogenesis, depending on the sensory organ type. Neither E(spl) nor Su(H) seem to be involved in the N pathway that directs the neuron/glia choice in the PNS.

    N activity is suggested to be directly involved in cell proliferation, independently of its role in the formation of the dorsal/ventral boundary.

    fng and N form a complex through both the Lin-Notch repeats and the epidermal growth factor repeats 22-36.

    The activation of Su(H) by N involves the release of Su(H) from an inhibitory complex which contains H.

    N is involved in a common regulatory pathway for the determination of the various Drosophila appendages.

    EGF-like repeats 11 and 12, the RAM-23 and cdc10/ankyrin repeats and the region C-terminal to the cdc10/ankyrin repeats of the N protein are necessary for both Dl and Ser proteins to signal via N. Dl and Ser utilise EGF-like repeats 24-26 of N for signalling, but there are significant differences in the way they utilise these repeats.

    N activity is required for sim expression in cellularising embryos.

    Endocytosis of the ligand Dl, complexed with the N extracellular domain, into signal-generating cells is required for separation of the N extracellular domain from the N intracellular domain.

    The effect of N on the development of the sensory macrochaetae is based on lateral inhibition while the effect of N on the longitudinal wing vein is of an inductive nature. (The development of ventral wing veins seems to be dependent on the inductive action of the dorsal surface veins).

    N protein responds differently to binding by Dl or wg protein. The Dl signal is transduced by the N intracellular domain released from the plasma membrane, the wg signal is transduced by the N intracellular domain associated with the plasma membrane.

    The composite signalling of the Ser and Dl genes through N patterns the segments of the leg, leading to the development of leg joints. Elsewhere in the tarsal segments, signalling by Dl and N is necessary for the development of non-joint parts of the leg.

    The Abruptex mutations of N disrupt the establishment of proneural clusters in Drosophila. This is not due to increased N signalling during lateral inhibition.

    Dl-mediated activation of N is required for establishment of ommatidial polarity; N signaling induces the R4 fate.

    The N signalling pathway in myogenesis appears to be organised in a similar way to neurogenesis.

    N signaling plays a crucial role in the singling out process of the fusion cell at the tip of each fusion branch in the developing tracheal system.

    In cultured cells, heterotypic interactions between N protein and the ligands Dl and Ser have higher affinities than homotypic interactions between Dl protein molecules.

    N acts directly in tracheal cells to distinguish individual fates within groups of equivalent cells. N helps single out those cells that mediate branch fusion by blocking their neighbors from adopting the same fate. N also acts in the selection of those cells that extend the terminal branches.

    Dl may activate N to specify cell fates at the tip of the developing tracheal branches.

    N is required for dorsoventral lineage restriction in wing imaginal discs.

    Nspl-1 specifically affects N inductive processes during eye development. Proneural cells are lost. Enhancement of the phenotype by E(spl)1 occurs within the remaining proneural cells, operating primarily at the protein level due to altered protein-protein interactions between E(spl)1 gene product and the proneural proteins.

    Candidate gene for quantitative trait (QTL) locus determining bristle number.

    Ca-P60A function is required for intracellular trafficking of the N receptor.

    The Dl ligand is cleaved at the cell surface, releasing an extracellular fragment capable of binding to N and acting as an antagonist of N activity.

    Local activation of N is necessary and sufficient to promote the formation of joints between segments of the leg. This segmentation process requires the participation of Ser, Dl and fng.

    N appears to act in a novel pathway in a wide range of tissues during Drosophila development.

    Proteosome-mediated protein degradation antagonizes N signalling activity, perhaps by targeting an active form of N protein for degradation.

    dpp and N specify the fusion cell fate in the dorsal branches of the developing trachea. The selection of single fusion cells from the dpp responsive cells is accomplished by the up-regulation of the Dl ligand in the presumptive fusion cells and the activation of the N receptor in the cells that remain at the stalk of the branch.

    Psn is required for activity and nuclear access of N.

    Psn is required for the proteolytic release of the intracellular domain of N following activation of N by ligand.

    Microtubules may be involved in mediating the antagonistic interaction between numb and N during RP2 and sib fate specification.

    The strong genetic interactions between N and wg is at least partly due to regulation of expression of cuticle patterning genes by wg and the two forms of N.

    N functions in the patterning of the dorsal epidermis and dorsal closure via a signalling activity carried out by N at the cell surface that does not require its cleavage and acts by modulating signal through the JNK pathway.

    The femoral chordotonal organ arises from a cluster of sensory organ precursors (SOPs). N signalling is required to limit SOP commitment in the development of this cluster, but does not prevent multiple SOP formation because of the antagonistic action of Egfr signalling. Egfr signalling is required for clustering, promoting SOP commitment rather than proliferation or protection from cell death.

    twi and N negatively regulate adult muscle differentiation in Drosophila.

    Cells neighboring the SMC do not acquire the neural fate because N signalling pathway effectors, the HLH proteins of the E(spl) complex, block the sc self-regulation loop.

    N is required to promote growth and set up the axis of mirror symmetry in the eye.

    N regulates three distinguishable processes in embryonic myogenesis; it autonomously controls the initial segregation of muscle progenitors from among competent myoblasts, subsequent to this founder cell identity remains sensitive to mesodermal N activity until myoblast fusion and additionally N can suppress muscle development by regulating a nonautonomous signal from the ectoderm.

    N signalling may regulate not only cell fates but also aspects of cell polarity at mitosis.

    The requirement for N in axon patterning reflects a function of the protein at the time of axon outgrowth, genetically separable from the role of N in the establishment of cell identities.

    The Dab and Abl gene products may play a role in N signalling in axons, perhaps by binding to the N intracellular domain.

    Six EMS-induced alleles have been isolated that suppress the macrochaetae, microchaetae and wing vein phenotypes of NAx-16.

    Activation of the N receptor in the wing disc induces strong mitotic activity. The effect of N on cell proliferation is not simply due to the upregulation of either vg or wg. On the contrary, vg and wg proteins show synergistic effects with N signaling, resulting in the stimulation of cell proliferation in imaginal discs.

    Activation of the N receptor in the wing disc induces the expression of vg and wg.

    Loss of function N mutations are neuralizing but gain of function mutations are anti-neuralizing in epidermal clones; both are lethal in gynandromorphs. An extra dose of wild type N fully restores the viability of the gynandromorphs. Lethal Abruptex-class mutations are viable in clones in the eye as well as the cuticle. Clones induced in the third larval instar are less viable than those induced in the first instar, due to the antineurogenic effect of Abruptex mutations.

    In wing development, wg, in conjunction with N, induces G1 and G2 arrest in separate subdomains of the zone of non-proliferating cells at the developing wing margin. The wg product induces G2 arrest in two subdomains by inducing ac and sc, which down-regulate stg. N activity creates a third domain by preventing arrest in G2 in wg-expressing cells resulting in their arrest in G1.

    N is processed in a ligand-dependent manner to generate a phosphorylated cytoplasmic domain that preferentially associates with Su(H). Localization studies suggest that the relative levels of Su(H), Dl and N regulate nuclear entry of the N/Su(H) complex. N behaves as a transcriptional transactivator in the nucleus.

    vg is involved in the specification of the wing primordia under the combined control of N and wg signalling. Once cells are assigned to the wing fate, their development relies on a sequence of regulatory loops that involve N, wg and vg. During this process, cells that are exposed to the activity of both wg and vg will become wing blade and those that are continuously under the influence of wg alone develop as hinge. The growth of the cells in the wing blade results from a synergistic effect of the three genes N, wg and vg on the cells that have been specified as wing blade.

    Evidence suggests that intracellular processing of N occurs in embryos in a Dl-dependent manner.

    The signal promoting survival of cells in the interommatidial lattice is part of a balance between N and Ras85D pathways, which appear to act in opposition to regulate the number of interommatidial cells permitted to remain. N directs programmed cell death in the interommatidial lattice.

    N functions in both the standard lateral inhibition pathway and in a second independent pathway to influence mesodermal cell fates in the embryo.

    spdo and N act in opposition to numb to distinguish sibling neuron fates in the CNS.

    The intracellular domain of the N product gains access to the nucleus in response to ligand, possibly through a mechanism involving proteolytic cleavage from the remainder of the protein. Signal transduction by N depends on the ability of the intracellular domain, containing the CDC10 repeats, to reach the nucleus and participate in the transcriptional activation of the target genes.

    N activation at segment boundaries in the leg is critical for the formation of joints and also affects the growth of each leg segment.

    An autonomous requirement for N signalling makes retinal cells competent for R8 differentiation, this requirement precedes the role of N in lateral inhibition of differentiation. N has sequentially opposite effects in the same cells, by first promoting and then inhibiting proneural gene function. The competence of retinal cells to differentiate as R8 cells and the inhibition of differentiation in response to later N signalling is itself induced by N.

    In the absence of N function neural differentiation does not occur.

    Genetic analysis of N mutants suggests that there are functionally different classes of N alleles that affect different steps in the development of the peripheral nervous system. In particular one class affects a function of N in the establishment of proneural clusters, while other classes interfere with the role of N during lateral inhibition.

    Genetic combinations with mutants of nub cause additive phenotypes.

    N-inducible expression of HLHmδ and HLHmγ both in cultured cells and in vivo is dependent on functional Su(H) protein.

    Dominant interactions indicate that toc is acting in the same signalling pathways for the formation of the egg chamber as da, N and Dl.

    Ser ligand binding to N is a necessary but insufficient step toward N activation.

    Feedback regulation is central to Dl-N signalling required for wing vein morphogenesis.

    Ser can activate or inactivate N in a concentration-dependent manner. While inactivation is likely to be mediated by a dominant negative effect over N, the activation is similar to that elicited by Dl and requires the product of the Su(H) gene.

    N, but not wg signalling, is autonomously required for ct expression.

    The ventral neurogenic primordium of N embryos has been transplanted into the neural tube of amphibian and mammalian embryos. Morphological and functional contacts are established between the transplanted cells and the host brain tissue, suggesting incorporation of insect nerve cells into the brain of vertebrates.

    When wild-type N is activated by its ligand Dl, shi is required in both signaling and receiving cells for normal singling out of precursors.

    Overexpression of different constitutively active forms of N in shi mutant flies indicates that shi function is not necessary for transduction of the signal downstream of N, even when the receptor (N) is integrated in the plasma membrane.

    The secreted forms of the Dl and Ser gene products are antagonists of N signalling in the developing eye and wing.

    N is required to specify the es fate, since in N- conditions only md neurons are produced. This is true in the mixed and solo es lineages suggesting that all ASC-dependent precursors have the potentiality to produce md neurons and the N+ function is required in all types of ASC-dependent lineages to specify the es alternative.

    Su(H) is required for only a subset of the asymmetric divisions that depend on the function of numb and N.

    N function is required at the dorsoventral boundary of the developing wing for its normal growth and patterning. The combined effect of N and its target genes ct and wg regulate the expression of N ligands Dl and Ser which restrict N signalling to the wing dorsoventral boundary.

    N is involved in determining vein thickness in wing development.

    The establishment of vein thickness depends on independent regulation of N and Dl expression in intervein and vein territories, N activation by Dl in cells where N and Dl expression overlaps, positive feedback on N transcription in cells where N has been activated, repression of rho transcription by HLHmβ and maintenance of Dl expression by rho/Egfr activity.

    dsh interacts antagonistically with N and Dl.

    The dsh product physically interacts with the carboxy terminus of that of N.

    dsh, in addition to transducing wg signal, blocks N signalling directly, explaining the inhibitory cross-talk observed between the pathways.

    N is required autonomously by mesoderm cells to establish the proper ratio of muscle founders. N-Dl signaling between mesoderm cells may limit the number of muscle founders by a pathway analogous to lateral inhibition of neurogenesis in the ectoderm.

    ato expression is coupled to N signalling only at a critical autoregulatory stage. Results propose that transitions between successive phases of proneural gene expression are important for neuronal pattern formation.

    In the absence of N, wg signaling appears to occur normally, arguing against a direct role for N in wg signaling.

    N-expressing cells in a given compartment have different responses to Dl and Ser. Dl and Ser function as compartment-specific signals in the wing disc, to activate N and induce downstream genes required for wing formation.

    ro acts in conjunction with the more ubiquitously used N regulatory pathway.

    brn and egh, originating from the germline, collaborate with N on the apical surface of follicle cells to mediate germline-follicle cell adhesion.

    Overexpression of numb in N mutants demonstrates a synergistic interaction suggesting that numb and N function in the same genetic pathway.

    Yeast two-hybrid interaction assay is used to demonstrate a direct protein-protein interaction between N and numb.

    Proneural and neurogenic genes control specification and morphogenesis of stomatogastric nerve cell precursors.

    E(spl)-C mutants are epistatic over a gain of function mutant of N.

    N plays a role in oogenesis in differentiation of follicle cells by holding them in a precursor stage of development.

    Constitutively active N causes follicle cell fate defects opposite to those generated by a loss of function allele of N and causes a defect in the organisation of the microtubules within the oocyte which implicates information from the follicle cells in regulating this organisation.

    There is no interaction between sca and N (or Dl) proteins.

    A hierarchical relationship between N, wg and vg patterns the dorsoventral axis of the wing.

    rst expression and sorting of interommatidial cells is affected by N facet mutations.

    Su(H) directly participates in N lateral signalling during sensory organ precursor (SOP) specification.

    N, H and Su(H) exhibit dose-dependent genetic interactions.

    dMP2 and vMP2 neurons express N and adjacent cells express Dl.

    Intracellularly truncated forms of Ser and Dl behave as dominant-negative proteins in an apparently non-cell autonomous manner. The presence of intracellular domains is essential for proper N ligand function in the eye.

    Phenotypes of N loss of function alleles indicate different requirements in dorsal and ventral cells. Ser and Dl, two N ligands, have asymmetrical requirements at the dorsal-ventral boundary during wing development. Su(H) and E(spl) are required for all aspects of N function at the wing dorsoventral boundary.

    The genes of the E(spl) complex mediate only a subset of N activities during imaginal development. Comparisons of mutant phenotypes suggests that the N pathway bifurcates after the activation of Su(H) and that E(spl) activity is not required when the consequence of N function is the transcriptional activation of downstream genes. Transcriptional activation mediated by Su(H) and transcriptional repression mediated by E(spl) could provide greater diversity in the response of individual genes to N activity.

    The integrity of multiple Su(H) binding sites found in the proximal upstream region of E(spl) complex genes and Su(H) activity are required for transcriptional response to hyperactivity of the N receptor. Su(H) is a direct regulatory link between N receptor activity and the expression of E(spl) complex genes, extending the known lineage of the N cell-cell signaling pathway.

    Deregulated activity of the N receptor prevents the establishment of the SOP cell fate, just as loss of H+ function does.

    The process of singling out individual l(1)sc expressing cells in the mesoderm fails to occur in N and Dl mutants.

    Induction of vg requires the combined activities of Ser, wg and N. Based on the patterns of expression and requirements for Ser and wg during initiation wing development it is proposed that Ser is a dorsal signal and that wg is a ventral signal. Their combination at the dorso-ventral interface activates the N receptor and leads to vg expression.

    N signalling in the wing directs wg expression in the wing dorsal/ventral boundary. In the wing activation of N, mediated through Su(H), is sufficient to direct wg expression.

    The wg and N signalling pathways interact to define the range of lateral inhibition within the SNS anlage, causing the selection of the three ac expressing cells instead of one.

    Invagination centers within the somatogastric nervous system anlage are positioned by N-mediated signaling which is spatially controlled though wg.

    Expression of Ser leads to N-dependent suppression of ac expression in proneural clusters. Results suggest that Ser functions as an alternative ligand capable of N activation.

    In late stages of development E(spl) BHLH gene products are part of the same signalling pathway and are expressed in cells where N is activated. Loss of N function leads to a reduction in E(spl) bHLH protein expression and the presence of ubiquitous activated N result in high levels of E(spl) bHLH throughout the developing wing disc, effects are independent of genes of the AS-C.

    Amorphic mutations of z are strong recessive enhancers of position effect variegation (PEV) for the w, rst and N loci.

    Examination of the ac expression and the sensory mother cell arrangement in N mutations demonstrates that processes of cellular and molecular interactions mediated by N gene products are responsible for the establishment of stripes of ac expression.

    N receptor activity suppresses H function during adult external sense organ development. H activity insulates sensory organ precursor cells from inhibition by N. H function appears to be an integral negative regulatory element of the N signalling pathway.

    The dx gene product functions in N signalling as a positive regulator, that acts genetically upstream of N.

    dx plays a role in the N signaling pathway.

    Genetic interactions suggest that cno participates with members of the N pathway in regulating adhesive cell-cell interactions for the determination of cell fate.

    N is required within the zone of wg expression along the D/V boundary to establish or maintain wg expression, this loss of wg expression in N- clones may be partially or wholly responsible for the antiproneural N phenotype.

    Observations from N- wing clones support the hypothesis that N is required on the margin for distinct processes. N is required for the properly patterned segregation of SMCs from the proneural region.

    N proteins have similar functions in vertebrates and invertebrates (Chitnis et al., 1995, Nature 375: 761 and Henrique et al., 1995, Nature 375: 787).

    The sub-transmembrane region of N, structurally equivalent to the amino terminal part of mRAM23, is involved in the interaction with Su(H).

    Genetic interaction analysis suggests a three way interaction between Su(dx), dx and N.

    Genetic interaction and phenotypic analysis suggest that the product of wg is a ligand for N during pattern formation in the embryo and the imaginal discs.

    Protein binding and genetic studies implicate dx in the N signalling pathway.

    In cultured Drosophila cells, the Su(H) product is sequestered in the cytoplasm when coexpressed with N protein and is translocated to the nucleus when N protein binds its Dl protein ligand. N activity may regulate nuclear events by controlling the activity of a DNA-binding protein.

    Su(H) shows allele specific interactions with N, Dl, dx and mam.

    The migration of wing glial cells is affected by N and fu, which both affect axonogenesis, suggesting that the two processes are tightly associated.

    N is necessary for the implementation of the wg signal in specifying normal wing development.

    N signalling activity is directly responsible for the accumulation of basic helix-loop-helix proteins encoded by the E(spl) locus.

    Mutants display an embryonic neoplastic phenotype.

    The N product is required for midline development in the embryo, and is necessary for the activation of sim. The midline is required to allow commissure formation in the CNS.

    Genetic and phenotypic analysis suggests that the Abruptex class of N mutations cause stronger than normal N activation by the Dl product. The Abruptex phenotypes are modified by mutations at Ser, Dl, H and gro.

    There are three different N requirements in the wing: in imaginal disc cell proliferation, in restriction of vein differentiation and in margin formation. N activity during epidermal cell proliferation and wing vein differentiation is exerted by its regulation of a common group of genes involved in the specification and restriction of vein competent regions.

    The expression patterns of N and Dl are highly regulated both spatially and temporally, and are similar, though do not coincide directly during a number of stages of oogenesis.

    N is a neurogenic gene required initially to ensure the correct number of PNS precursors. N continues to be required in the peripheral ectoderm, possibly for maintenance of the commitment to an epidermal fate.

    Duplication of N rescues many of the defects of sno mutants. Mutations at sno rescue a phenotype resulting from the overexpression of N.

    Overexpression of wild type N gene in defined cell types has no apparent effect but overexpression of activated N in the same cells transiently blocks their proper cell fate commitment causing them to adopt incorrect cell fates or to differentiate incompletely.

    The N and Dl gene products play a role in axon guidance of the intersegmental nerve. Expression of Dl on a branch of the trachea provides a path, and the axons use the N protein on their surfaces to recognise the path. A similar mechanism specifies the trajectory of part of the axonal scaffold of the CNS.

    Temperature shift experiments demonstrate that N has two separable effects on cells of the embryonic visual system. First, it delimits the number of cells recruited into the presumptive Bolwig's organ. Secondly, N is necessary for cells of the optic lobe to remain an epithelium.

    In addition to the binding of N molecules on one cell to the Dl molecules of apposing cells, the N and Dl proteins on the surface of the same cell may interact, altering the availability of these proteins to interact with their counterparts on adjacent cells.

    N and Dl expression are generally coincident within developing tissues. At the subcellular level, Dl and N are localized in endocytic vesicles during down regulation from the surfaces of interacting cells, consistent with their roles as signal and receptor.

    Analysis of deletion mutants generated in vitro suggests that N functions as a receptor whose extracellular domain mediates ligand binding, resulting in the transmission of developmental signals by the cytoplasmic domain. The cdc10/ankyrin repeat region plays an essential role in the signal transduction events.

    Analysis of deficiencies reveals that N and Dl are required for migration of the endoderm and its transition to an epithelium.

    sgg is part of a signalling pathway downstream of N.

    N plays no role in the emergence of the proneural clusters, but is involved in limiting the number of cluster cells that differentiate as SMCs.

    The intracellular portion has intrinsic activity and that the extracellular domain functions to regulate the activity.

    Truncated forms of the N protein cause cell fate transformations in vivo.

    A new allele of Notch, NM1, has been isolated that behaves genetically as both an antimorph and a loss of function allele:the basis for the antimorphism lies in the titration of Notch wild type products into NM1/N+ nonfunctional dimers and/or the titration of Delta products into non-functional ligand-receptor complexes.

    Mutation of N is found using the gene titration method to search for genes involved in the determination of sense organs. The mutation of N demonstrates an interaction with Df(4)M101-62f, a chromosome known to alter the development of the PNS.

    Gene dosage studies demonstrate that N and Dl proteins interact at the membranes of adjacent cells.

    The N gene functions with dx in developmental pathways to specify cell fate.

    At least for ectodermally and endodermally derived tissues, neurogenic gene function is primarily involved in interactions among cells that need to acquire or maintain an epithelial phenotype.

    The N+ protein is expressed in cells destined for neural and epidermal lineages and also in mesodermal cells. Later N expression is restricted to the neuroblasts and their derivatives, the neurons and nerve processes.

    The expression of the N phenotype depends on the dosage of N+, two doses in females and one in males being essential to produce wild-type flies. N includes phenotypically distinct regions 'N'(Notch), 'Ax' (Abruptex), 'Co' (Confluens), 'fa' (facet), 'l(1)N' (lethal (1) Notch), 'nd' (notchoid) and 'spl' (split). Complementation between alleles can be understood as due to the spatial or temporal separation of defects in the course of development. The defects occur throughout developmental stages from embryo to late pupa. Mutant alleles of the Notch group: Wings of heterozygotes incised at tips and often crowded along edges; veins L3 and L5 thickened; thoracic microchaetae and irregularly distributed. Males and homozygous females are lethal. In some N mutants, the phenotype is mild and varies in one or more of its typical features, but such N's can usually be identified by phenotypes expressed when heterozygous with recessive visible eye and wing mutants that also occur at N. Females N/N+ show the Notch phenotype; females N/N+; Dp(1;2)51b (representing a duplication for the N locus) are wild type. In the hemizygous male, N/Y is lethal, whereas N/Y;Dp(1;2)51b is viable and phenotypically normal; the wild phenotype is dependent upon the presence of the normal dosage of 3C6-7 for each sex. An extra dose of 3C6-7, as in Dp(1;2)51b or Dp(1;1)Co, causes the expression of the dominant phenotype Confluens (Co); thus N+/N+;Dp(1;2)51b Mutant alleles of the Abruptex group: In the Ax group of mutations homozygous females and males show shortened L5 vein, usually also L4, L2, and sometimes L3. Wings shortened, arched and thin. Costal bristles clumped and frayed; costal veins thickened. Thorax shows midfurrow with rearranged hair directions; hairs on thorax and head fewer, with clear patches and streaks. Male genitalia often rotated. Three classes of Ax mutations can be distinguished: Some alleles (NAx-16, NAx-71d and NAx-E2) in heterozygous combination with N enhance the wing-incision phenotype; others (NAx-1 and NAx-9) suppress wing incision of N and in turn display suppression wing-vein gapping by N; yet another class (NAx-59b and NAx-59d) are homozygous lethal. N-enhancing and N-suppressing alleles are homozygous viable, but lethal when heterozygous with each other. Mutant alleles of the Confluens group: NCo is a duplication that affects wing veins when expressed in homo- and hemizygotes. Mutant alleles of the facet group: The recessive visible 'fa' and 'spl' mutants affect the surface of the eye; in heterozygotes with N, the eyes are rough. Facet mutants affect the texture of the eye and in some cases cause slight to moderate wing nicks. Until now some recessive mutations with wing nicking but with normal eye texture have been designated as alleles of fa based upon their not being complemented by N mutants; in this treatment their designations have been changed to nd: notchoid, since they fail to complement nd mutants and like nd alleles, they complement fa alleles. All fa alleles complement spl, another eye-texture mutant in the N locus. facet alleles show two general phenotypes, facet and glossy: the facet phenotype has rough eyes owing to irregularities in size, shape and arrangement of ommatidia; eye color is uniform and wild type. The glossy phenotype also displays irregular facets, but the eye surface is smooth and pigment distribution may be uneven. Mutant alleles of the lethal (1) Notch group: There are four phenotypic classes of l(1)N alleles: (1) Those that are lethal with N and wild type with the recessive visibles <up>Nl1N-1</up>; (2) Those that are lethal with N but not wild type with the recessive visibles <up>Nl1N-2, Nl1N-3</up>; (3) Alleles whose heterozygotes with N+ have a phenotype not recognized as Notch <up>Nl1N-B</up>, or (4) Alleles that are temperature sensitive for lethality and do not express a Notch phenotype in heterozygotes with N+ <up>Nl1N-ts1</up>. Mutant alleles of the notchoid group: In the notchoid group of mutations the wings are notched and the veins thickened. Homozygotes are viable and fertile in both sexes. About 10% of Nfa-1/Nnd-1 flies have small notches in one or both wings. Nnd-3/Nnd-1 heterozygotes have slightly thickened wing veins with deltas; Nspl-1/Nnd-1 heterozygotes lack a few bristles (like Nspl-1/+) and their eyes are sometimes smaller than normal and roughened. Nspl-1,Nnd-1 males have rough eyes, nd-like wings an

    The N locus is involved in the differentiation of the ectoderm. The wild-type allele of N is essential for the proper development of the neurogenic region, appearing to direct some ectodermal elements into the epidermal pathway of development.

    Dl passes on the lateral inhibitory signal from one cell to another via its physical interaction with the receptor trans-membrane protein N.

    N mutants shows neural hypertrophy in nau-expressing cells. The clusters enlarge so much that they merge to form longitudinal rows on either side of the midline. Clusters of βTub85D-producing cells also enlarge and merge together but they cannot assume correct morphology as they don't fuse properly, they are also displaced.

    In the absence of N, sensory mother cells appear in the correct location and in well defined clusters.

    Neurogenic loci like N are required to restrict the number of competent cells that will become SMCs.

    N is required for the segregation of normal numbers of neural precursors and for the differentiation of the bristle organ. Clonal analysis demonstrates that N gene product is required for the mechanism of choosing alternative cell fates: N acts as a receptor for an inhibitory signal emanating from the neural precursors.

    The N 36 EGF repeats form a tandem array of discrete ligand-binding units, each of which may potentially interact with several different proteins during development.

    N may act as a multifunctional receptor.

    N function is essential in early midoogenesis. Mosaic analysis revealed that N is required in the soma for several processes of oogenesis, including proper bcd localization in the oocyte.

    Lack-of-function alleles of N exaggerate ASC "Hw" phenotypes in both ectopic and normal positions.

    N is required for the singularization of sensory organ mother cells in chaetogenic regions and subsequent chaeta differentiation.

    Mutations in N affect early ommatidial development.

    Suppressing effects of Dlsup4 and Dlsup5 are N allele specific.

    N has haploinsufficient phenotype of thickened veins.

    Fas3, mys, disco, zip, l(2)gl, N and Egfr mutants show an additive phenotype in combination with Fas1TE89Da.

    An in vitro aggregation assay demonstrates that expression and interaction of N and Dl in cultured cells causes cell aggregation, this aggregation is calcium-dependent.

    Mitotic recombination experiments reveal that the N product is required by epidermal cells subsequent to neuroblast delamination.

    The products of vg and sca act in conjunction with N, in a dosage sensitive manner, to stimulate the differentiation of specific cell types.

    An extra wild type copy of N, in combination with dxENU, suppresses the wings nicks and thickened veins, and partially suppresses the ocellar phenotype.

    Dl mutations can modify the imaginal phenotypes that result from heterozygosity for N mutations.

    The eye abnormalities of spl mutants are the result of abnormal differentiation of photoreceptors at the morphogenetic furrow.

    In loss-of-function alleles of tkv, N and Dl, thickened veins and occasional plexi are seen, associated with small wings. In gain-of-function alleles the reciprocal phenotype is seen, associated with large wings. The Notch phenotypic group includes neurogenetic mutations involved in cell communication. Some alleles are embryonic lethal.

    N, Dl and E(spl) gene products interact directly during embryonic and imaginal development.

    Morphogenesis of the ectodermally derived adult eye is sensitive to the combined action of the N, Dl and E(spl) gene products.

    A study of the interactions between N, Dl, H and E(spl) suggest that the effects of H, Dl and E(spl) on N are allele specific and occurring at the protein level.

    Neural hyperplasia, caused by mutations in N, can be prevented by the presence of another neurogenic mutation.

    Triploidy for N leads to a reduction in the severity of the neur- phenotype, this is not a reciprocal relationship. Increasing number of wild type copies of N does not modify the bib phenotype. N- embryos lacking maternal and zygotic expression are no different to N- embryos lacking only the zygotic component in the presence of H-, or duplications of neur+ or E(spl)+.

    N expression is generalized and not confined to tissues affected by mutant alleles.

    Phenotypic effects are context-specific.

    Single N-/0 cells transplanted to N+ recipient embryos can give rise to hypoderm.

    Sensillum differentiation in peripheral nervous system of mutant embryos is abnormal.

    N acts autonomously in hypodermal (epidermal) cells.

    400bp HindIII SalI fragment that maps between coordinates +8.96 and +9.36 contains the opa-e. opa-e is composed of repeating units of CAX triplet where X is either G or A.

    opa-e is found between amino acids 2537 and 2567 in region IV of the N protein, located after the transmembrane domain. opa-e extends for 30 amino acids and is a stretch of almost pure glutamine residues.

    The notching in notchoid mutants is found mostly on anterior and posterior margins and is the result of cell death.

    N mutants display hypertrophy of the nervous system and the ventral cuticle is absent.

    opa-e is found between coordinates +8 and +9.5 within the N locus. N transcripts can be detected in unfertilized eggs.

    The expression of genes controlling neurogenesis is dependent on the previous activity of the genes controlling the development of the embryonic dorsal-ventral pattern.

    opa-e can be found between coordinates +7.8 and +8.3 within the N locus.

    There is a maternal component of N expression.

    Recessive lethal and visible N mutants alter activities of four enzymes of the mitochondrial respiratory chain.

    A 'spl' stock from Novosibirsk, Russia, shows temperature sensitivity.

    The 'spl' bristle phenotype is caused by an extra division of an initial bristle-forming cell.

    Temperature sensitive periods for defects in N mutants have been identified.

    'Ax' mutants show dominant wing and bristle phenotypes distinct from 'Notch' mutants.

    Homozygotes and hemizygotes for all N mutants suffer the same embryological defects. Both presumptive hypoderm and presumptive neuroblasts develop as neuroblasts, resulting in embryos with a hypertrophied central nervous system lacking ventral and ventral-lateral hypoderm.

    'l(1)N' mutants do not show a Notch phenotype over N+.

    split mutants behave autonomously in mosaics in regard to both eye and bristle phenotypes.

    N+/N+;Dp(1;2)51b females and N+/Y;Dp(1;2)51b males are Co-like. The notchoid mutants show notched-wings and thickened veins.

    The notchoid mutants show notched-wings and thickened veins.

    Thoracic microchaetae are crowded and irregularly distributed.

    N/N+ females show notched wings and vein and microchaetal abnormalities. Thoracic microchaetae are crowded and irregularly distributed.

    Relationship to Other Genes
    Source for database merge of
    Additional comments

    "l(1)G0275" may affect "N".

    Ectopic expression of Mmus\Mfng or Mmus\Rfng in Drosophila results in phenotypes that resemble those seen in N mutants.

    Nomenclature History
    Source for database identify of

    Source for identity of: N CG3936

    Nomenclature comments
    Etymology

    The name "Notch" comes from the appearance of notches in wing tips in females homozygous or heterozygous for certain mutant alleles.

    Synonyms and Secondary IDs (38)
    Reported As
    Symbol Synonym
    EG:140G11.1
    EG:163A10.2
    N
    (Arias and Tomlinson, 2025, Li et al., 2025, Mukherjee et al., 2025, Ribeiro et al., 2025, Shun Li et al., 2025, Singh et al., 2025, Yun et al., 2025, Collins et al., 2024, Jang et al., 2024, Ko et al., 2024, Li et al., 2024, Megaly et al., 2024, Reimels et al., 2024, Saez-Carrion et al., 2024, Wilkin et al., 2024, Wu et al., 2024, Attrill, 2023, Bharti et al., 2023, Burghardt et al., 2023, Carter et al., 2023, Chen et al., 2023, Heigwer et al., 2023, Mari et al., 2023, Pan et al., 2023, Rosales-Vega et al., 2023, Titlow et al., 2023, Troost et al., 2023, Voutyraki et al., 2023, Yu et al., 2023, Ayukawa et al., 2022, Corrales et al., 2022, Ding et al., 2022, Gera et al., 2022, Hultmark and Andó, 2022, Jullien et al., 2022, Kharrat et al., 2022, Koca et al., 2022, Langridge et al., 2022, Li et al., 2022, Logeay et al., 2022, Nurmahdi et al., 2022, Ray and Li, 2022, Schnute et al., 2022, Theodorou et al., 2022, Volkova et al., 2022, Voutyraki et al., 2022, Zhang and Edgar, 2022, Zhao 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et al., 2005, Baonza and Freeman, 2005, Bardot et al., 2005, Eissenberg et al., 2005, Emery et al., 2005, Firth and Baker, 2005, Galindo et al., 2005, Gao et al., 2005, Hayward et al., 2005, He et al., 2005, Hori et al., 2005, Jafar-Nejad et al., 2005, Moberg et al., 2005, Moon et al., 2005, Mukherjee et al., 2005, Nagel et al., 2005, Peel et al., 2005, Pérez et al., 2005, Roederer et al., 2005, Somers and Chia, 2005, Sotillos and De Celis, 2005, Stella et al., 2005, Thomas, 2005, Thompson et al., 2005, Vaccari and Bilder, 2005, Wech and Nagel, 2005, Wei et al., 2005, Zhang et al., 2005, Ahimou et al., 2004, Baker, 2004, Brodu et al., 2004, Kamimura et al., 2004, Kamimura et al., 2004, Loewer et al., 2004, Loewer et al., 2004, Loop et al., 2004, MacDougall et al., 2004, Markstein et al., 2004, Merdes et al., 2004, Pyrowolakis et al., 2004, Lei et al., 2003, Li et al., 2003, Micchelli et al., 2003, Michellod et al., 2003, Wesley and Mok, 2003, Duvic et al., 2002, Martinez Arias, 2002, Rath et al., 2002, Portin, 2001, Presente et al., 2001, Trachtulec and Forejt, 2001, Gorski et al., 2000, Indrasamy et al., 2000, Giebel, 1999)
    Notch
    (Dong and Cheng, 2025, Barbaste et al., 2023, Guichard et al., 2023, Markey et al., 2023, Ortega-Campos and García-Heredia, 2023, Zhu et al., 2023, Enomoto and Igaki, 2022, Lacoste et al., 2022, Marchetti et al., 2022, Boukhatmi, 2021, Casares and McGregor, 2021, Dombrovski and Condron, 2021, Harnish et al., 2021, Jafari and Alenius, 2021, Lam Wong and Verheyen, 2021, Lee et al., 2021, Loganathan et al., 2021, Saiki et al., 2021, Strutt and Strutt, 2021, Sun et al., 2021, Zmojdzian and Jagla, 2021, Antel and Inaba, 2020, Chen and Desplan, 2020, Cui et al., 2020, Haudry et al., 2020, Ishibashi et al., 2020, Kamdem et al., 2020, Serafini et al., 2020, Yamamoto, 2020, Jeong et al., 2019, Laddada et al., 2019, Meltzer et al., 2019, Bala Tannan et al., 2018, Yao et al., 2018, Basu et al., 2017, Bradley-Gill et al., 2016, Matsumoto et al., 2016, Padash Barmchi et al., 2016, Zacharioudaki et al., 2016, Aradhya et al., 2015, Kohlmaier et al., 2015, Palmer et al., 2015, Córdoba and Estella, 2014, Parsons et al., 2014, Zhang et al., 2014, Bergstralh et al., 2013, Farca-Luna and Sprecher, 2013, Hombría and Sotillos, 2013, Jennings, 2013, Levayer and Moreno, 2013, Morin-Poulard et al., 2013, Noatynska et al., 2013, Woodfield et al., 2013, Yamamoto-Hino and Goto, 2013, Zhang et al., 2013, Zoranovic et al., 2013, Amoyel and Bach, 2012, Bier and Guichard, 2012, Burke, 2012, Engel et al., 2012, Fausti et al., 2012, Kapuria et al., 2012, Kelsom and Lu, 2012, Saini and Reichert, 2012, Tieu et al., 2012, Troost and Klein, 2012, Whitworth et al., 2012, Xu and Gridley, 2012, Apidianakis and Rahme, 2011, Crozatier and Vincent, 2011, Eliazer and Buszczak, 2011, Juarez et al., 2011, Laprise, 2011, Miles et al., 2011, Jiang et al., 2009, Bardin et al., 2008, Krisel and Moberg, 2007, Zinzen and Papatsenko, 2007, Chan et al., 2005, Park et al., 2003)
    anon-EST:Liang-1.12
    l(1)3Cb
    l(1)Ax
    l(1)N
    Name Synonyms
    Chopped
    Confluens
    Notch
    (Shi et al., 2026, Adell et al., 2025, Geng et al., 2025, Gujar and Wang, 2025, Liu et al., 2025, Marcetteau et al., 2025, Park et al., 2025, Röper, 2025, Sarkar et al., 2025, Shafer, 2025, Wu et al., 2025, Fenelon et al., 2024, Jiang, 2024, Kasirer and Sprinzak, 2024, Larnerd et al., 2024, Liang and Luan, 2024, Luo et al., 2024, Mattila et al., 2024, Megaly et al., 2024, Parambath et al., 2024, Pfefferkorn et al., 2024, Pinot and Le Borgne, 2024, Reddy Onteddu et al., 2024, Sachan et al., 2024, Sood et al., 2024, Tam and Rand, 2024, Tsukamoto et al., 2024, Veneti et al., 2024, Verma et al., 2024, Wang et al., 2024, Wang et al., 2024, Weng et al., 2024, Zhao et al., 2024, Baldenius et al., 2023, Carter et al., 2023, Delanoue et al., 2023, Josserand et al., 2023, Petsakou et al., 2023, Pollington et al., 2023, Roy et al., 2023, Sharpe et al., 2023, St Johnston, 2023, Townson et al., 2023, Zhai et al., 2023, Agrawal and Tuthill, 2022, Almeida Machado Costa et al., 2022, Beghelli et al., 2022, Daly et al., 2022, Gagliani et al., 2022, Hegde and Srivastava, 2022, Ho et al., 2022, Irion and Nüsslein-Volhard, 2022, Jia et al., 2022, Jiang et al., 2022, Junion and Jagla, 2022, Kimble and Nüsslein-Volhard, 2022, Koranteng et al., 2022, Liu et al., 2022, Milas and Telley, 2022, Papagiannouli, 2022, Revici et al., 2022, Rout et al., 2022, Soares et al., 2022, Wang et al., 2022, Xiao, 2022, Xiu et al., 2022, Yasugi and Sato, 2022, Zhao et al., 2022, Al Hayek et al., 2021, Bahuguna et al., 2021, Bailey et al., 2021, Boumard and Bardin, 2021, Brás et al., 2021, Charlton-Perkins et al., 2021, Del Río and Montaner, 2021, Falo-Sanjuan and Bray, 2021, Gama-Brambila et al., 2021, Gan et al., 2021, Girard et al., 2021, Gong et al., 2021, Harrison et al., 2021, Hartenstein et al., 2021, Hayes and Melrose, 2021, Hounjet and Vooijs, 2021, Hung et al., 2021, Lim et al., 2021, Meng and Heckscher, 2021, Missirlis, 2021, Morin-Poulard et al., 2021, Park et al., 2021, Rajan et al., 2021, Rambur et al., 2021, Reiff et al., 2021, Riddiford et al., 2021, Rossi et al., 2021, Shi et al., 2021, Weterings et al., 2021, Zhang et al., 2021, Zhao et al., 2021, Aradhya and Jagla, 2020, Arzate-Mejía et al., 2020, Bahrampour and Thor, 2020, Bai and Suzuki, 2020, Córdoba and Estella, 2020, Das et al., 2020, Denton et al., 2020, Díaz-de-la-Peña et al., 2020, Dutta et al., 2020, Feng et al., 2020, Funk et al., 2020, Gerlach and Herranz, 2020, Girard et al., 2020, Graves et al., 2020, Jin et al., 2020, Khan et al., 2020, Lan et al., 2020, Laurichesse and Soler, 2020, Lee et al., 2020, Li et al., 2020, Lin and Hsu, 2020, Luo et al., 2020, Maurange, 2020, Maurya et al., 2020, Merkle et al., 2020, Nishihara, 2020, Parasram and Karpowicz, 2020, Perez-Gomez et al., 2020, Poovathumkadavil and Jagla, 2020, Reichrath and Reichrath, 2020, Rust and Nystul, 2020, Şahin et al., 2020, Sato and Yasugi, 2020, Tamamouna et al., 2020, Ulgherait et al., 2020, van Soldt and Cardoso, 2020, Vlachakis et al., 2020, Wei et al., 2020, Yaghmaeian Salmani and Thor, 2020, Yoo et al., 2020, Zhao et al., 2020, Zhou and Boutros, 2020, Bäumers et al., 2019, Chen et al., 2019, Flint Brodsly et al., 2019, Gahr et al., 2019, Guo et al., 2019, Hunter et al., 2019, Jörg et al., 2019, Laddada et al., 2019, Lee and Chen, 2019, Maier, 2019, Ng et al., 2019, Rajaei et al., 2019, Ramon-Cañellas et al., 2019, Reinhardt et al., 2019, Singh et al., 2019, Viswanathan et al., 2019, Wan et al., 2019, Wu et al., 2019, Alfred and Vaccari, 2018, Bellec et al., 2018, Boulet et al., 2018, Hayashi and Kondo, 2018, Kato et al., 2018, Kim and Jho, 2018, Losada-Perez, 2018, Ly et al., 2018, Ogawa et al., 2018, Paul et al., 2018, Peiris et al., 2018, Petrovsky and Großhans, 2018, Richardson and Portela, 2018, Ruiz-Losada et al., 2018, Salazar and Yamamoto, 2018, Schaeffer, 2018, Schwartz and Rhiner, 2018, Wissel et al., 2018, Yin and Xi, 2018, Zhang et al., 2018, Ahmad, 2017, An et al., 2017, Chaturvedi et al., 2017, Costa et al., 2017, Dai et al., 2017, Gervais and Bardin, 2017, Hong et al., 2017, Jin et al., 2017, Khare et al., 2017, Kojima, 2017, Langridge and Struhl, 2017, Lee, 2017, Li et al., 2017, Liu and Jin, 2017, Liu and Jin, 2017, Liu et al., 2017, Liu et al., 2017, Losada-Perez et al., 2017, Loubéry et al., 2017, Schell et al., 2017, Szuplewski et al., 2017, Tauc et al., 2017, Varshney and Stanley, 2017, Xie et al., 2017, Xu et al., 2017, Zaytseva and Quinn, 2017, Barton et al., 2016, Chen et al., 2016, Clavería and Torres, 2016, Golovin and Broadie, 2016, Hegedűs et al., 2016, Hudry et al., 2016, Johnston et al., 2016, Kayser and Biron, 2016, Kitagawa, 2016, Losada-Perez et al., 2016, Ma et al., 2016, Mavromatakis and Tomlinson, 2016, Mbodj et al., 2016, Okumura et al., 2016, Reid and O'Brochta, 2016, Saadin and Starz-Gaiano, 2016, Schwartz et al., 2016, Takashima et al., 2016, Wieschaus and Nüsslein-Volhard, 2016, Yadav et al., 2016, Zacharioudaki et al., 2016, Albuquerque et al., 2015, Aparicio et al., 2015, Aradhya et al., 2015, Arlotta and Hobert, 2015, Arya et al., 2015, Auer et al., 2015, Beehler-Evans and Micchelli, 2015, Buchon and Osman, 2015, Contreras et al., 2015, Enomoto et al., 2015, Erdmann et al., 2015, Imai et al., 2015, Irvine and Harvey, 2015, Ishio et al., 2015, Lu and Li, 2015, Matsuno et al., 2015, Nie et al., 2015, Ogawa et al., 2015, Palmer and Deng, 2015, Pasco et al., 2015, Reimels and Pfleger, 2015, Ren et al., 2015, Rice et al., 2015, Ryoo, 2015, Schweisguth, 2015, Vlisidou and Wood, 2015, Wang et al., 2015, Wangler et al., 2015, Yu et al., 2015, Zhai et al., 2015, Alaña et al., 2014, Bao, 2014, Bertet et al., 2014, Brockmann et al., 2014, Cantera et al., 2014, Charng et al., 2014, Cheruiyot et al., 2014, Gersten et al., 2014, Gómez-Lamarca et al., 2014, Gunage et al., 2014, Hassel et al., 2014, Heimiller et al., 2014, Housden et al., 2014, Issman-Zecharya and Schuldiner, 2014, Jones and Srivastava, 2014, Kornberg and Roy, 2014, Li et al., 2014, Loubéry and González-Gaitán, 2014, Loubéry et al., 2014, Loza-Coll et al., 2014, Mishra et al., 2014, Montagne and Gonzalez-Gaitan, 2014, Ntziachristos et al., 2014, Oliveira et al., 2014, Parsons et al., 2014, Pézeron et al., 2014, Skwarek et al., 2014, Takáts et al., 2014, Tognon et al., 2014, Wang et al., 2014, Wurmbach and Preiss, 2014, Xie et al., 2014, Zacharioudaki and Bray, 2014, Zhang et al., 2014, Aoyama et al., 2013, Babaoğlan et al., 2013, Bonn et al., 2013, Chen et al., 2013, Christiansen et al., 2013, Cridland et al., 2013, Das et al., 2013, Fleming et al., 2013, Giagtzoglou et al., 2013, Groth et al., 2013, Hermle et al., 2013, Kanda et al., 2013, Katoh and Tiemeyer, 2013, Koch et al., 2013, Langen et al., 2013, Lee et al., 2013, Lerner et al., 2013, Lin et al., 2013, Maier et al., 2013, Marianes and Spradling, 2013, Markstein, 2013, Mbodj et al., 2013, Müller et al., 2013, Neckameyer and Argue, 2013, Pepperl et al., 2013, Perdigoto and Bardin, 2013, Pérez-Gómez et al., 2013, Petzoldt et al., 2013, Pitsouli and Perrimon, 2013, Ronen et al., 2013, Roti et al., 2013, Sachan et al., 2013, Schaaf et al., 2013, Schneider et al., 2013, Shim et al., 2013, Stine and Matunis, 2013, Sun and Spradling, 2013, Terriente-Felix et al., 2013, Tremmel et al., 2013, Upadhyay et al., 2013, van de Hoef et al., 2013, Weasner and Kumar, 2013, Weavers and Skaer, 2013, Whiteman et al., 2013, Willoughby et al., 2013, Wong et al., 2013, Xin et al., 2013, Xiong et al., 2013, Yang et al., 2013, Yousefian et al., 2013, Zeng et al., 2013, Zhan et al., 2013, Zhang et al., 2013, Zhou and Haddad, 2013, Zhou and Luo, 2013, Barth et al., 2012, Bejarano et al., 2012, Cheng et al., 2012, Couturier et al., 2012, Dornier et al., 2012, Giagtzoglou et al., 2012, Gomez et al., 2012, Guruharsha et al., 2012, Haenfler et al., 2012, Homem and Knoblich, 2012, Housden et al., 2012, Kametaka et al., 2012, Krzemien et al., 2012, Legent et al., 2012, Majumder et al., 2012, Mitra et al., 2012, Moraru et al., 2012, Ochoa-Espinosa and Affolter, 2012, Pallavi et al., 2012, Peng et al., 2012, San Juan et al., 2012, Singh and Mlodzik, 2012, Tepass, 2012, Troost et al., 2012, Ulvklo et al., 2012, Weber et al., 2012, Weng et al., 2012, Wong et al., 2012, Xiao et al., 2012, Xie et al., 2012, Yamakawa et al., 2012, Yamamoto et al., 2012, Zhang et al., 2012, Zhu et al., 2012, Alattia et al., 2011, Andersson et al., 2011, Baker and Firth, 2011, Banks et al., 2011, Benhra et al., 2011, Bhat et al., 2011, Boggiano et al., 2011, Bonner and Boulianne, 2011, Cave et al., 2011, Chen et al., 2011, Dahmann et al., 2011, Dalton et al., 2011, Daskalaki et al., 2011, Djiane et al., 2011, Duan et al., 2011, Egoz-Matia et al., 2011, Eliazer et al., 2011, Endo et al., 2011, Feng et al., 2011, Glavic et al., 2011, Halbsgut et al., 2011, Hwang and Rulifson, 2011, Jiang et al., 2011, Kato et al., 2011, Klusza and Deng, 2011, Kurth et al., 2011, Kuzina et al., 2011, Kvon et al., 2011, Lee 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2003, Zweifel et al., 2003, Martinez Arias, 2002, Rath et al., 2002, Dawes-Hoang and Wieschaus, 2001, Kitagawa et al., 2001, Portin, 2001, Presente et al., 2001, Smith, 2001, Struhl and Greenwald, 2001, Gorski et al., 2000, Indrasamy et al., 2000, Wesley, 1999, Weinmaster, 1997, Stifani et al., 1992, Kidd, 1989.3.15, Wharton, 1989.6.15)
    notchoid
    strawberry
    Secondary FlyBase IDs
    • FBgn0000311
    • FBgn0002916
    • FBgn0017616
    • FBgn0024967
    • FBgn0026804
    Datasets (0)
    Study focus (0)
    Experimental Role
    Project
    Project Type
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    Study result (0)
    Result
    Result Type
    Title
    External Crossreferences and Linkouts ( 287 )
    Sequence Crossreferences
    NCBI Gene - Gene integrates information from a wide range of species. A record may include nomenclature, Reference Sequences (RefSeqs), maps, pathways, variations, phenotypes, and links to genome-, phenotype-, and locus-specific resources worldwide.
    RefSeq - A comprehensive, integrated, non-redundant, well-annotated set of reference sequences including genomic, transcript, and protein.
    UniProt/GCRP - The gene-centric reference proteome (GCRP) provides a 1:1 mapping between genes and UniProt accessions in which a single 'canonical' isoform represents the product(s) of each protein-coding gene.
    UniProt/Swiss-Prot - Manually annotated and reviewed records of protein sequence and functional information
    UniProt/TrEMBL - Automatically annotated and unreviewed records of protein sequence and functional information
    Other crossreferences
    AlphaFold DB - AlphaFold provides open access to protein structure predictions for the human proteome and other key proteins of interest, to accelerate scientific research.
    BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
    DRscDB - A single-cell RNA-seq resource for data mining and data comparison across species
    EMBL-EBI Single Cell Expression Atlas - Single cell expression across species
    FlyAtlas2 - A Drosophila melanogaster expression atlas with RNA-Seq, miRNA-Seq and sex-specific data
    FlyMine - An integrated database for Drosophila genomics
    KEGG Genes - Molecular building blocks of life in the genomic space.
    MARRVEL_MODEL - MARRVEL (model organism gene)
    PDB - An information portal to biological macromolecular structures
    Linkouts
    BioGRID - A database of protein and genetic interactions.
    Drosophila Genomics Resource Center - Drosophila Genomics Resource Center (DGRC) cDNA clones
    DroID - A comprehensive database of gene and protein interactions.
    DRSC - Results frm RNAi screens
    Developmental Studies Hybridoma Bank - Monoclonal antibodies for use in research
    FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
    FlyCyc Genes - Genes from a BioCyc PGDB for Dmel
    Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
    Flygut - An atlas of the Drosophila adult midgut
    iBeetle-Base - RNAi phenotypes in the red flour beetle (Tribolium castaneum)
    Interactive Fly - A cyberspace guide to Drosophila development and metazoan evolution
    KEGG Pathways - A collection of manually drawn pathway maps representing knowledge of molecular interaction, reaction and relation networks.
    MIST (genetic) - An integrated Molecular Interaction Database
    MIST (protein-protein) - An integrated Molecular Interaction Database
    SignaLink - A signaling pathway resource with multi-layered regulatory networks.
    References (3,593)