General Information
Symbol
Dmel\N
Species
D. melanogaster
Name
Notch
Annotation Symbol
CG3936
Feature Type
FlyBase ID
FBgn0004647
Gene Model Status
Stock Availability
Gene Snapshot
In progress.Contributions welcome.
Also Known As
Notch, Ax, spl, fa, NICD
Genomic Location
Cytogenetic map
Sequence location
X:3,134,870..3,172,221 [+]
Recombination map
1-2
Sequence
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
GO Summary Ribbons
Families, Domains and Molecular Function
Gene Group Membership (FlyBase)
Protein Family (UniProt, Sequence Similarities)
Belongs to the NOTCH family. (P07207)
Molecular Function (see GO section for details)
Summaries
UniProt Contributed Function Data
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:15620650, PubMed:12909620, 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:27151950, PubMed:28899667, PubMed:20152183, PubMed:18342578, PubMed:23056424, PubMed:21262215).
(UniProt, P07207)
Phenotypic Description from the 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
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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.
Gene Model and Products
Number of Transcripts
2
Number of Unique Polypeptides
1

Please see the GBrowse view of Dmel\N or 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
Comments on Gene Model
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.52
Sequence Ontology: Class of Gene
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
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 Dl via the EGF repeats and the Dl EGF repeats. Interacts with Nedd4 and Su(dx). Interacts with O-fut1; the interaction glycosylates N and transports N to early endosomes.
(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:12909620, PubMed:10935637). O-glucosylation by rumi in the endoplasmic reticulum is necessary for correct folding and signaling (PubMed:18243100). Ubiquitinated by Nedd4; which promotes ligand-independent endocytosis and proteasomal degradation. May also be ubiquitinated by Su(dx).
(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
Gene Ontology (141 terms)
Molecular Function (4 terms)
Terms Based on Experimental Evidence (2 terms)
CV Term
Evidence
References
inferred from direct assay
inferred from physical interaction with FLYBASE:Su(H); FB:FBgn0004837
inferred from physical interaction with UniProtKB:E1JHA6
inferred from physical interaction with FLYBASE:dx; FB:FBgn0000524
inferred from physical interaction with UniProtKB:Q9VVI3
(assigned by UniProt )
inferred from physical interaction with FLYBASE:Dl; FB:FBgn0000463
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
(assigned by UniProt )
inferred from physical interaction with UniProtKB:Q9Y0H4
(assigned by UniProt )
inferred from physical interaction with FLYBASE:shg; FB:FBgn0003391
Terms Based on Predictions or Assertions (2 terms)
CV Term
Evidence
References
inferred from electronic annotation with InterPro:IPR001881, InterPro:IPR018097
(assigned by InterPro )
traceable author statement
non-traceable author statement
Biological Process (124 terms)
Terms Based on Experimental Evidence (91 terms)
CV Term
Evidence
References
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with UniProtKB:Q9VQ56
(assigned by UniProt )
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 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
(assigned by UniProt )
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
(assigned by UniProt )
inferred from mutant phenotype
inferred from direct assay
inferred from genetic interaction with FLYBASE:nerfin-1; FB:FBgn0028999
inferred from mutant phenotype
(assigned by UniProt )
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:Cdk9; FB:FBgn0019949
inferred from mutant phenotype
inferred from mutant phenotype
(assigned by UniProt )
inferred from mutant phenotype
(assigned by UniProt )
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:scrib; FB:FBgn0263289
inferred from mutant phenotype
(assigned by UniProt )
inferred from genetic interaction with UniProtKB:P51023
(assigned by UniProt )
inferred from genetic interaction with UniProtKB:P51023,UniProtKB:Q9VQ56
(assigned by UniProt )
inferred from genetic interaction with UniProtKB:Q9VQ56
(assigned by UniProt )
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 (40 terms)
CV Term
Evidence
References
traceable author statement
traceable author statement
non-traceable author statement
traceable author statement
non-traceable author statement
traceable author statement
traceable author statement
traceable author statement
non-traceable author statement
traceable author statement
non-traceable author statement
traceable author statement
non-traceable author statement
non-traceable author statement
non-traceable author statement
traceable author statement
traceable author statement
non-traceable author statement
non-traceable author statement
Cellular Component (13 terms)
Terms Based on Experimental Evidence (12 terms)
CV Term
Evidence
References
inferred from direct assay
inferred from direct assay
inferred from direct assay
colocalizes_with cytoplasmic vesicle
inferred from direct assay
inferred from direct assay
inferred from direct assay
inferred from direct assay
colocalizes_with late endosome
inferred from direct assay
colocalizes_with lysosome
inferred from direct assay
inferred from direct assay
colocalizes_with nucleus
inferred from direct assay
inferred from physical interaction with FLYBASE:Su(H); FB:FBgn0004837
inferred from direct assay
Terms Based on Predictions or Assertions (2 terms)
CV Term
Evidence
References
inferred from electronic annotation with InterPro:IPR010660, InterPro:IPR011656
(assigned by InterPro )
traceable author statement
non-traceable author statement
traceable author statement
Expression Data
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.
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.
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 direct assay
inferred from direct assay
inferred from direct assay
colocalizes_with cytoplasmic vesicle
inferred from direct assay
inferred from direct assay
inferred from direct assay
inferred from direct assay
colocalizes_with late endosome
inferred from direct assay
colocalizes_with lysosome
inferred from direct assay
inferred from direct assay
colocalizes_with nucleus
inferred from direct assay
inferred from physical interaction with FLYBASE:Su(H); FB:FBgn0004837
inferred from direct assay
Expression Deduced from Reporters
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
High-Throughput Expression Data
Associated Tools

GBrowse - Visual display of RNA-Seq signals

View Dmel\N in GBrowse 2
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
FLIGHT - Cell culture data for RNAi and other high-throughput technologies
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
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 Phenotypes
Classical and Insertion Alleles ( 366 )
For All Classical and Insertion Alleles Show
 
Allele of N
Class
Mutagen
Associated Insertion
Stocks
Known lesion
    0
    --
      0
      Yes
      0
      --
        0
        Yes
          0
          --
          0
          --
            0
            Yes
              0
              --
                0
                --
                  0
                  --
                    0
                    Yes
                      0
                      --
                        0
                        --
                          0
                          --
                            0
                            --
                              0
                              --
                                0
                                --
                                  0
                                  --
                                    0
                                    --
                                      0
                                      --
                                        0
                                        --
                                          0
                                          --
                                            0
                                            --
                                            Other relevant insertions
                                            insertion of mobile activating element
                                            Name
                                            Expression Data
                                            miscellaneous insertions
                                            Name
                                            Expression Data
                                            Transgenic Constructs ( 240 )
                                            For All Alleles Carried on Transgenic Constructs Show
                                            Transgenic constructs containing/affecting coding region of N
                                            Allele of N
                                            Mutagen
                                            Associated Transgenic Construct
                                            Stocks
                                            Transgenic constructs containing regulatory region of N
                                            UAS construct
                                            reporter construct
                                            Name
                                            Expression Data
                                            Deletions and Duplications ( 180 )
                                            Disrupted in
                                            Not disrupted in
                                            Summary of 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
                                            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 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