Ax, spl, NICD, fa, Abruptex
transmembrane receptor - neurogenic - responsible for lateral inhibition and cell fate choices
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AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.52
10.2 (unknown)
10.4 (sequence analysis)
10.5 (northern blot)
11.7 (northern blot)
2703 (aa)
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).
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).
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.
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.
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).
Comment: periphery of embryo
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.
Comment: ectodermal cells
Comment: elevated
Comment: elevated
Comment: elevated
Comment: elevated
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 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.
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 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.
JBrowse - Visual display of RNA-Seq signals
View Dmel\N in JBrowse1-2
1-2.5
1-2.7 +/- 0.2
1-3.0
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.
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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.
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.
monoclonal
polyclonal
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 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.
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.
N signalling contributes to long term memory formation in the adult brain.
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.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
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 endogenous N gene is rearranged in S2 cells.
N is required for the genesis of a subset of glial cells in the CNS.
N activity is suggested to be directly involved in cell proliferation, independently of its role in the formation of the dorsal/ventral boundary.
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.
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.
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.
N appears to act in a novel pathway in a wide range of tissues during Drosophila development.
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.
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.
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.
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.
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.
N functions in both the standard lateral inhibition pathway and in a second independent pathway to influence mesodermal cell fates in the embryo.
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.
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.
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.
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.
Proneural and neurogenic genes control specification and morphogenesis of stomatogastric nerve cell precursors.
N plays a role in oogenesis in differentiation of follicle cells by holding them in a precursor stage of development.
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.
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.
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.
N proteins have similar functions in vertebrates and invertebrates (Chitnis et al., 1995, Nature 375: 761 and Henrique et al., 1995, Nature 375: 787).
Mutants display an embryonic neoplastic phenotype.
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 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.
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.
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.
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 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
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.
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.
N has haploinsufficient phenotype of thickened veins.
Mitotic recombination experiments reveal that the N product is required by epidermal cells subsequent to neuroblast delamination.
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.
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.
Sensillum differentiation in peripheral nervous system of mutant embryos is abnormal.
N acts autonomously in hypodermal (epidermal) cells.
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.
The expression of genes controlling neurogenesis is dependent on the previous activity of the genes controlling the development of the embryonic dorsal-ventral pattern.
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.
Source for identity of: N CG3936
The name "Notch" comes from the appearance of notches in wing tips in females homozygous or heterozygous for certain mutant alleles.