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General Information
Symbol
Dmel\N55e11
Species
D. melanogaster
Name
FlyBase ID
FBal0012701
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Notch55e11, N55ell
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Polytene chromosomes normal (Welshons).
Nature of the lesion
Statement
Reference
3.5kb insertion in the 5' coding region that causes premature termination of transcripts.
Insertion upstream of EGF repeats.
Insertion in 5' coding region: premature termination of transcripts.
Insertion of a copia-like element at coordinate -26kb (coordinates according to FBrf0045027 and FBrf0039003).
Insertion components
?{}N55e11
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
follicle cell & nucleus | somatic clone
fusion competent cell & visceral mesoderm
macrochaeta & scutum | somatic clone
muscle founder cell & visceral mesoderm
scutum & macrochaeta | ectopic (with Df(1)N-8)
socket & scutum | somatic clone
Detailed Description
Statement
Reference
N55e11 heterozygotes show wing margin loss and wing vein thickening, which are more severe at 30[o]C than at 25[o]C; one additional copy of Ngt-16-20 leads to partial wing vein loss.
N55e11 follicle cell clones show a loss of polar/stalk cells, as compared to controls.
N55e11 heterozygosity does not significantly affect the number or size of third instar larval circulating crystal cells.
N55e11 heterozygous adults display supernumerary thoracic sensory bristles, as compared to controls.
N55e11 heterozygous adult flies display wing vein deltas and extra scutellar bristles.
The wings of N55e11/+ mutant adults are significantly smaller than those of wild type flies.
N55e11/+ flies have a notch between L3 and L4 in 56% of wings.
N55e11 mutant flies display vein thickening phenotype as well as ectopic venation.
N55e11/Y ; Ngt-4-35 animals raised at 18[o]C do not show a rhabdomere attachment phenotype.
The majority of N55e11 heterozygous females show notched wings, which are not seen in wild type controls, with half of flies having one notch and a small minority having multiple notches.
N55e11/N55e11 clones in the third instar lymph gland induce lamellocyte differentiation outside of the clone boundary.
N55e11 mutant female germline stem cells (GSCs) do not undergo the natural turnover seen in wild type: at three weeks after clone induction more N55e11 mutant GSCs are still present in the niche in comparison with wild type controls. The contact area between N55e11 mutant female germline stem cells and the niche is greater than in wild type controls.
Heterozygotes have a wing notching phenotype (20% of flies have a single nick in the margin at the distal tip.
N55e11/+ adults display a wing-notching phenotype.
55% of homozygous N55e11 single cell dorsal cluster neuron clones innervate the medulla, compared to only 24% of control clones.
Heterozygotes show wing vein thickening and wing margin defects.
Heterozygous females show notching of the distal wing.
N55e11 homozygous lateral antennal lobe neuroblast clones, induced at the newly-hatched larval stage, have fewer antennal mechanosensory and motor center neurite projection tracts and 5 times the number of uniglomerular lateral antennal lobe projection neurons in the adult with no evidence for overall altered number of neurons.
N55e11/+ flies show normal eye and thorax morphology.
Homozygous type II neuroblast clones show premature loss of neuroblasts.
N55e11/+ wings show a very mild wing defect.
Midguts from N55e11 heterozygotes at 10 days of age show abnormal intestinal stem cell to enteroblast ratio, imbalanced towards the former.
N55e11/+ females display a decrease in the number of ovarian niche cap cells.
N55e11/+ adult flies have one trichogen (hair) and one tormogen (socket) cell per notal microchaeta, similar to wild-type controls.
In N55e11/+ flies, thickening of wing veins and wing margin loss are observed.
N55e11 heterozygotes exhibit mild expansion of the L3 wing vein.
Homozygous clones in the outer proliferation center neuroepithelium (induced at late-first or early-second instar and analysed at late-third instar) adopt rounded or irregular cell morphology rather than the normal columnar epithelial cell morphology in 57.9% of cases.
No anterior midline glial cells (AMG) are seen in N55e11 mutant embryos at either stage 13 or stage 16. N55e11 mutant stage 16 embryos contain six MP1 neurons per segment compared to the two seen in wild type. The H cell sib cell is absent and the number of H cells is increased to 10, compared to only one in wild type. N55e11 mutant stage 16 embryos contain 11 mVUM cells per segment, compared to three in wild type. The iVUM and MNB cells appear to be absent.
N55e11 clones induced in the lateral neuroblast lineage (lNb) at the larval stage (0-4 hours after hatching) can give rise to all of the neurons that are normally generated by this lineage, produce clones containing the normal number of cells. N55e11 clones show a significant reduction in the number of local interneurons (LNs) and total absence of acj6-positive atypical projection neurons (aPNs) with a concomitant increase in the number of GH146-positive projection neurons (PNs) compared to wild type, when analysed at the adult stage.
Heterozygotes show a wing nicking phenotype.
Clones of homozygous N55e11 mutant cells induced in early L1 larvae and analysed at late L3 lack a discernible peripheral cell. Mutant islands tend to merge together. The lack of peripheral cells does not seem to affect adult midgut progenitor divisions.
Heterozygotes show thickening of the wing veins.
N55e11 clones generated early in development are never recovered in the wing disc; with later inductions the number and size of mutant clones increases, but not to wild type levels.
Transplanted N55e11 donor NB1-1 cells exhibit major changes compared to wild-type. As in wild-type, two neurons in a dorsal position within the nerve cord are detected, where normally the aCC/pCC neurons are located. However, the axonal projections of these cells are both typically aCC-like and innervate the dorsal muscle 1 (DO1), suggesting a duplication of the aCC neuron at the expense of the pCC neuron. Cells with pCC-like projections could not be detected in N55e11 clones. In N55e11 mutant NB1-1 lineage clones, the typical subperineural glial components are lost, with this loss always being accompanied by a gain of neurons within the interneuronal cluster. In some cases, the fascicle of the posterior projections seem to contain more axons as judged from an increased size of the fascicle. N55e11 mutant MP2 clones exhibit a vMP2 to dMP2 cell fate transformation. N55e11 mutant NB4-2 lineage clones exhibit duplication of the RP2 neurons at the expense of its siblings RP2sibs. The duplication of these dorsal cells is accompanied by the loss of the ventral RP2 sib neurons. In addition, the 4-2MN projections are entirely missing in these clones. Approximately 80% of N55e11 mutant NB7-1 lineage clones exhibit a complete loss of U-neurons. The remaining 20% exhibit at least one U-neuron motor axon, resulting in the fascicles leaving the CNS appearing thinner. Thicker fascicles are observed running through the anterior and posterior commissures in some clones, potentially indicating the presence of more interneurons, possibly U-sib neurons.
Follicle stem cell clones homozygous for N55e11 persist in the ovariole approximately as well as control clones over a 14 day period. Egg chamber fusions are seen in ovarioles containing homozygous follicle stem cell clones.
One copy of N55e11 results in wing nicking, slight broadening of the veins at the tips (deltas) and occasional duplication of the scutellar macrochaetae.
Over 90% of male stage 8 embryos derived from heterozygous N55e11 females crossed to wild type males display neurogenic phenotypes. Cuticle defects are seen that range from no cuticle, through to spiracles and mouth hooks only to partial cuticle. Only around 5% of embryos have denticles.
Heterozygotes show distal wing notching.
Homozygous intestinal stem cell (ISC) clones in the adult midgut form tumours.
Mutant stage 9 embryos show neuroblast hyperplasia and elevated mitotic activity in the developing neuroectoderm. Heterozygous females have an ectopic bristle phenotype.
The number of fusion competent myoblasts is decreased in stage 11 N55e11 embryos.
Homozygous clones in the adult midgut result in two types of phenotype; either they give rise to growing clusters of diploid enteroendocrine-like cells (which express pros) or they give rise to a mass of diploid cells that do not express pros.
N55e11 mutant germline stem cells are maintained in the niche similarly to wild-type control clones.
Somatic clones of N55e11 in mid-third instar larvae have normal numbers and distribution of postembryonic neuroblasts.
N55e11 germline clones and N55e11 zygotic mutants exhibit crystal cells.
Homozygous follicle cell clones can result in fused egg chambers containing 32 germline nuclei. These egg chambers contain 2 oocyte nuclei suggesting that they probably result from fusion of two distinct cysts. These fused egg chambers have polar cells only at the termini of the fused cysts.
In N55e11 homozygous embryos, the early steps of proventricular development including the formation of the ball-like evagination at the ectoderm/endoderm boundary occur normally. However, at stage 14, the anterior boundary cells of the keyhole region fail to invaginate into the endodermal cell layer, but arrest anteriorly and do not move inwards until the final stages of embryonic development (16 and 17). In addition, the posterior boundary cells of the endodermal component of the proventriculus rim collapses in these animals.
Female flies heterozygous for N55e11 show moderate scalloping of the wing, thickened wing vein L3, and duplicated anterior and posterior scutellar macrochaetae.
Mutant embryos show severe hyperplasia of the central and peripheral nervous systems.
Marker expression and morphology suggest that numbers muscle founder cells are increased at the expense of fusion competent myoblasts in the visceral mesoderm of stage 11 N55e11 mutant embryos.
Heterozygotes have a wild-type bristle pattern.
In heterozygous mutants, wing veins are wider than in wild-type, but selection of sensory organ precursors (SOP) is not affected. However, the campaniform sensillae are still overlapping the posterior-most L3 vein cells. The position of SOPs relative to the anterior posterior border is not changed in mutant discs, indicating that in the adult the position of L3 vein is shifted anteriorly by one or two rows of cells.
Heterozygotes show a slight increase in the density of microchaetae on the notum.
The number of crystal cell precursors seen in mutant lymph glands is significantly reduced.
When mitotic follicle cell N55e11 mutant clones completely surround an egg chamber, this egg chamber fuses, partially or completely, to the adjacent wild-type anterior cyst but not to the posterior one. The stalk is unable to form at the anterior of cysts with N55e11 mutant follicle cells, where these fusions occur. The oocyte is always correctly positioned in cysts that contain large posterior N55e11 follicle cell clones, even though these lack posterior polar cells. In contrast, the oocyte of wild-type cysts that are fused to chambers with N55e11 mutant follicle cells is frequently mispositioned. This mispositioning causes the oocyte to develop a reversed anterior-posterior axis.
N55e11/+ mutant flies have notches in the wing margin. These notches are more pronounced when flies carry the Df(3L)Ar14-8 deficiency.
Heterozygotes lack vein and sensory bristle tissue at the most distal tip of the wing.
Mutant embryos completely lack hindgut boundary cell rows and rings.
In mutant clones in the follicle cells the organization of the spectrin cytoskeleton is normal.
N55e11/Nl1N-ts1 flies form ectopic abdominal ventral multidendritic neurons and pI external sensory organ precursor cells, even when raised at 19oC.
The vMP2 neuron is transformed in a dMP2 neuron in transplanted N55e11 mutant MP2s.
N mutant embryos have about 89 cells in each Malpighian tubule cell (as opposed to about 125 in wild-type). The tubules are shorter than wild-type which results from a dramatic reduction in cell division from Mitosis 17. N mutant embryos made as germ-line clones have about 89 cells in each Malpighian tubule cell (as opposed to about 125 in wild-type).
At the earliest stage of the dorsal bipolar dendritic (dbd) sensory organ precursor (SOP) division excess nub-positive cells are located at the correct position in mutant embryos, suggesting that supernumerary dbd SOPs are produced. At stage 12, the dbd support glial cell (DBDG) is absent. Supernumerary PG3 glial cells and chordotonal organ ligament cells of the are present.
Cells in homozygous follicle cell clones have smaller nuclei than their wild-type neighbours (which probably indicates a lack of endocycles in the mutant cells). The mutant clones contain more cells than their wild-type twin spot sister clones, indicating additional mitoses. The mean ratio of the number of cells in the mutant clone/number of cells in the wild-type sister clone is 1.8 and the ratio does not change as a function of clone size. The DNA content is higher in wild-type sister clones than in mutant clones and the wild-type cells are larger on average than the mutant cells. The apical-basal polarity of mutant follicle cell clones appears to be normal.
Follicles containing permanent somatic clones for N55e11 are not recoverable. In egg chambers with transient somatic clones at either end of the follicle polar cells are absent. Where one of the polar-stalk precursors is mutant for N55e11 long stalks (average 15 cells) develop.
Homozygous somatic clones in the follicle cells do not differentiate as polar cells, but block the differentiation of epithelial follicle cells and causes them to remain as undifferentiated precursors. When a clone falls in a region where the follicle cells normally undergo morphogenetic movement, these movements do not occur. The stretched follicle cells fail to move over the nurse cells; the centripetal cells do not migrate between the oocyte and the nurse cells; and the more posterior follicle cells fail to move over the oocyte. No somatic clones in the stalk cells or the polar follicle cells are recovered. Occasionally, clones in the follicle cells leads to a failure of cyst encapsulation leading to fused or partially fused egg chambers. Homozygous mutant clones in the epithelial follicle cells are similar in size to wild-type twin spots, but contain many more smaller cells: the cells go through extra cell divisions, without a corresponding increase in growth rate. In wild type cells division ceases at stage 6, however mutant cells continue to divide up stages 10B or 11. Furthermore these cells have a lower DNA content indicating that mutant cells fail to switch from the mitotic cell cycle to the endo cycle and carry on dividing instead of becoming polyploid.
Pupal lethal when heterozygous with the MBT chromosome.
Glial cells in the central nervous system of embryos are not entirely absent. In clones of N55e11 cells in a wild type background the pCC is transformed into aCC, SPGs are lost and neuronal cells are concomitantly gained within the NB1-1 lineage.
Wing veins L3 and L5 are thicker than wild-type veins in heterozygous flies, and the thickened veins have smooth borders. The wings show moderate scalloping of the wing margin.
Nl1N-ts1/N55e11 flies exposed to the restrictive temperature during the third larval instar and pupal phases show a marked reduction in leg length with all areas of the leg segments (joint and interjoint tissue) being affected. Joints are completely lost, and also often apical bristles.
Mutants show a rudimentary tracheal tree, ectopic fusions between adjacent branches and absence of terminal branches. The number of tracheal cells is reduced, resulting in reduced branching. Temperature shifts of heterozygotes of N55e11/Nl1N-ts1 suggest that in addition to its early role in tracheal specification, N acts later in both fusion and terminal branching programs. Cell markers indicate a transformation of presumptive terminal or antifusion cells into fusion cells.
In somatic clones in the wing disc, the majority of N55e11 clones that are in contact with the ap boundary, disrupt the Dorsal/ventral (D/V) lineage restriction. In the most extreme class, clones straddle or cross the normal site of the D/V boundary from either side, with most or all of the cells being in the wrong compartment. In some cases milder distortions lead to "bulging" clones and some clones do approximately respect the boundary. Disruptions are not always limited to the mutant clone as in some cases the cells in the compartment adjacent to the N55e11 clone push into the compartment containing the clone. The severity of the abnormalities seen are greatest in clones generated at or just after the formation of the D/V restriction.
Nl1N-ts1/N55e11 wing discs show a reduction in the size of the pouch. Heterozygotes show mild notching of the distal wing margin.
Homozygous clones in the leg form patches of naked cuticle. The clones fail to form joint structures in all regions of the leg (resulting in fusion of leg segments) and leg growth is reduced. Fusions are seen along the length of the tibia and femur, while end-to-end fusions are seen in other leg segments. In most cases, the failure to form joints is an autonomous property of the mutant cells in the clone, although occasionally joint formation is also inhibited in wild-type cells that border a clone.
Homozygous mutant clones in the wing disc fail to respect the dorsal ventral boundary.
The number of ftz expressing MP2 neurons increases compared to wild-type (About 30 on each side of the midline, as compared to 2 in wild-type) in homozygous embryos derived from homozygous female germ-line clones (lacking both maternal and zygotic function). The extra MP2 clusters extend further laterally than seen in Dl and Su(H). alleles. No segmentation defects are seen. In homozygous embryos derived from homozygous female germ-line clones (lacking both maternal and zygotic function), clusters of 10 to 15 eve-expressing RP2-like cells are found in place of the normal RP2. These clusters often merge across the midline into a large cluster of 20 to 30 cells, apparently displacing or replacing the cell types that normally occupy the midline.
Leg discs of Nl1N-ts1/N55e11 larvae reared at the restrictive temperature for 4-16 hours show a large, disorganised mass of sensory organ precursor cells below the epithelium where the SOP cells of the femoral chordotonal organ normally form.
pb5/pb13 flies show a slight distal transformation of labium to antennal arista. If the flies are also heterozygous for N55e11 the number of pseudotracheal rows is reduced and a region of apparent ectoderm forms between the remaining pseudotracheal rows and the transformed antennal structures.
Multiple Malpighian tubule tip cells develop in homozygous embryos.
The segmental border muscle progenitors do not segregate at all or do not divide properly.
The cuticle of a Nl1N-ts1/N55e11 larva grown at 17oC until early stage 11 and then shifted to 30oC is shorter than wild-type and shows segment fusions.
Wing veins are thickened.
N55e11/Df(1)N-8 transheterozygotes exhibit ectopic bristles on the notum.
The number of cells in the nau-expressing muscle precursor clusters is increased compared to wild-type in homozygous embryos. The number of cells in the nau-expressing muscle precursor clusters is increased to more than twice the number in homozygous embryos (lacking zygotic function) in homozygous embryos derived from homozygous female germline clones (lacking both maternal and zygotic function).
Homozygous clones on the central region of the adult scutum are devoid of any external bristle structures, such as shafts and sockets. Homozygous clones induced in the sensory organ lineage frequently have bristles with double shafts (approximately 39% of homozygous macrochaetae have double shafts).
Hemizygous lethal. Heterozygotes have a neurogenic phenotype and have a marked increase in the number of bristles on the notum.
Scer\GAL4da.G32-mediated coexpression of l(1)scScer\UAS.cHa and daScer\UAS.cGa cause increase of cells in the CNS: brain lobes are enlarged (protruding through the holes in the cephalic epidermis), the ventral cord shows regional enlargement and sensory organs contain a large number of neurons. Neural hyperplasia is also increased, epidermis, fore- and hindgut, tracheal tree and salivary glands are completely neuralised.
Homozygous embryos have an increased number of cardiac precursor cells.
Segregation of neuroblasts 5-2 and 7-4 is normal at early stages. Late embryos are strongly neuralised. Embryos derived from germline clones exhibit disturbed segmentation in some segments and some 5-2 equivalence groups are fused. Segregation of the 5-2 and 7-4 neuroblast occurs in an irregular manner at later stages.
Heterozygotes show scalloping of the wing margin and thickening of the wing veins.
Transplantation of single cells from N55e11 embryos into the ventral neurogenic region of wild-type host embryos reveals non-autonomous behaviour of these cells; the cells can give rise to both neural and epidermal offspring. Single cells from N55e11 embryos transplanted into the ventral neurogenic region of N55e11 host embryos give rise to only neural cells. Single cells from N55e11 embryos transplanted into the procephalic neuroectoderm or the proctodeal anlage of wild-type host embryos generally adopt a neural fate. Single cells from N55e11 embryos transplanted into the ventral neurogenic region of host embryos derived from dl1 or dl2 mothers give rise to neural cells in 91% of cases. Single cells from wild-type embryos transplanted into the ventral neurogenic region of N55e11 host embryos give rise both neural and epidermal cells, at rates not significantly different from those obtained after transplantation of wild-type cells into wild-type hosts.
Embryos exhibit supernumerary md neurons that derive from ASC precursors.
Heterozygotes show thickening of the wing veins, occasional terminal nicking of the wing, and 1-4 ectopic bristles on the wing surface.
N55e11/+ flies have a notched wing phenotype. Homozygous clones induced in the sensory organ precursor daughter IIa cells of the adult external sense organs, when Scer\FLP1Scer\UAS.cBa expression is driven by Scer\GAL4sca-109-68, produce a twinned hair phenotype.
Heterozygotes exhibit no obvious hair or socket abnormalities. Heterozygotes carrying one copy of P{hs-numb} in the absence of heat shock have double hairs without sockets at the anterior wing margin. This phenotype is enhanced with two copies of P{hs-numb}.
Wing nicking phenotype.
Heterozygotes have a triangular expansion of the veins at the wing margin, and approximately 25% of flies have notched wings.
Clones in the thorax produce patches of naked cuticle, due to the differentiation of the ectopic SOPs into neurons. Clones in the wing that reach the wing margin show a loss of margin and blade tissue due to the requirement for N at the D/V boundary. Wing veins also appear thicker.
Instead of forming distinct invagination folds, the N mutant stomodeal nervous system anlage invaginates en masse.
SMC differentiation and proneural activation in N55e11 wing margin clones display dual phenotypes. Clones that do not substantially disrupt wg expression have neurogenic phenotypes and clones that disrupt wg expression have a mixture of antiproneural and neurogenic phenotypes.
Thickened vein mutant.
N55e11/Nl1N-ts1 animals reared at 17oC and exposed to 29oC for 24 hrs in the second larval instar give rise to adults with duplicated (sometimes triplicated) legs, with ventral branch points, and reduced or absent wings with accompanying wing to notum transformation. This phenotype is identical to that produced by loss of wg during second and early third larval instar. Heterozygosity for N55e11 reduces viability and increases penetrance of wing/haltere phenotypes of wg1. N, wg1 and arm4 triple mutants display, with about 10-20% penetrance, a perfect duplication of the notum charcateristic of wg mutations.
rl1/Df(2R)rl10a strongly enhances the wing phenotype of N55e11/+.
Embryos derived from germline clones show supernumerary Malpighian tubule tip cells segregating from the tubule primordial cells. The tubules of these embryos do not go on to secrete uric acid.
Mutant embryos rarely form commissural or longitudinal connections. Although the first axons grow out at the same time as wild-type axons, they are never oriented towards the midline, and even fail to form connections on the ipsilateral side. Both anterior and middle pairs of midline glia are absent, and the posterior pair are duplicated but found at ectopic positions. There are 4-8 additional neuronal midline cells per segment.
Clones running along the veins differentiate broad stretches of cells with vein histotype, to differentiate cells must be within 10-15 normal cell diameters from the vein. Clones can also affect vein differentiation on the other wing surface. Clones can also reduce the intervein distance. Clones in the dorso-ventral compartment border can induce scalloping indicating non-autonomous effects in wing margin loss. Clonal behaviour of N clones in the wing does not result from abnormal activity of the AS-C genes. px insufficiency does not improve the viability of N clonal cells.
Embryos exhibit few, if any, fused muscles. The unfused, birefringent fibres, have a random pattern of fine fibres apparently radiating out from small fragments of dorsal cuticle. The birefringent is clearly correlated with the expansion of the CNS and PNS, and the loss of epidermis and the degree to which myoblast fusion occurs. Where myoblast fusion fails conspicuous clusters of mesodermal cells are formed and if epidermal territories are expanded cells in these clusters may be recruited to fusion. Df(1)svr/N55e11 mutants show substantial rescue of both the cuticular and muscle phenotypes. The cuticle has expanded both in the anteroposterior and in the dorsoventral axes, although there is still no sign of denticle belts. Muscle phenotype shows many of the fibres are oriented and attached in a clearly patterned fashion. At the ventral margins of the cuticular shield the muscles appear disorganised with unfused fibres.
Hyperplasia of replicating sensory precursors: due to an increased number of ectodermal cells being recruited as sensory precursor cells. Extra precursor cells are recruited beyond the normal time window for neurogenesis in the PNS.
ac protein distribution in N55e11 embryos show ac expression is not restricted to a single cell of an ectodermal cell cluster, instead most cells of the cluster retain ac expression at a high level, enlarge, delaminate and become neuroblasts.
N55e11 shows severe neural hypertrophy, a 6--9 fold increase in nau expressing cells per cluster relative to wild type. Embryos show a disrupted CNS pattern. When heterozygous with Df(1)svr the CNS ladder structure is apparent, hypertrophy is seen in the nau expressing cells and the medial superclusters arise in a disrupted pattern compared to wildtype.
Increase in SMCs per cluster in embryos lacking the maternal product.
Neural hyperplasia of cells within a mutant clone. Mutant clones fail to form bristles.
Homozygous clones produced during the last stages of the formation of the adult sensory organs develop into sensory organ mother cells when induced early, or its neural sublineage later.
Cause a complex pleiotropic syndrome including perturbations of the chaetae pattern.
Post-transcriptional control of AS-C expression is suppressed, all cells expressing RNA accumulate protein.
The amount of maternally derived gene product does not modify the phenotype of double neurogenic mutants. N55e11 expression was modified by the presence of ASC loss-of-function mutations. All embryonic cells initiate neural development but later in development some cells switch their fate either to epidermogenesis or cell death.
Notching of the tips and/or edges of the wing. Veins are frequently broadened at the marginal junctions, forming delta-like thickenings.
The presence of the N55e11 did not affect the epidermal pattern in the thoracic and abdominal segments of hemizygotes derived from dl1/dl1 hemizygotes. Double mutants N55e11 and dl2 had neuralization of additional ectodermal cells in the thoracic and abdominal segments. Double mutants N55e11 and Tl had neuralization of the entire ectoderm, a huge CNS and no epidermis as it had been substituted for by neural tissue.
Extreme embryonic neurogenic phenotype.
Male flies carrying Dp(1;2)51bV76e show wing-notching and lateral incisions, leg defects and tarsal reductions, missing or multiple bristles, missing or fused ocelli and variegated or roughened eyes, at varying frequencies.
Lethal in combination with Nl1N-ts1 or NAx-tsl at 29oC.
A weak Notch. Deltas on wing veins are most reliable character for classification. Lethal when heterozygous with Nnd-3, 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).
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
N55e11 has visible | adult stage phenotype, enhanceable by Sirt1[+]/Sirt12A-7-11
N55e11 has visible | dominant | adult stage phenotype, enhanceable by p53[+]/p5311-1B-1
N55e11 has visible | dominant | adult stage phenotype, enhanceable by p535A-1-4/p53[+]
N55e11 has visible | dominant | adult stage phenotype, enhanceable by p53[+]/p53-ns
N55e11 has visible | dominant phenotype, enhanceable by dpn[+]/dpn1
N55e11 has visible | dominant phenotype, enhanceable by dpn[+]/dpn6
N55e11 has visible | dominant phenotype, enhanceable by sca[+]/scad09400
N55e11 has visible | dominant phenotype, enhanceable by klud00059/klu[+]
N55e11 has visible | dominant phenotype, enhanceable by lark[+]/lark1
N55e11 has visible | dominant phenotype, enhanceable by sm[+]/sm1
N55e11 has visible | dominant phenotype, enhanceable by sm[+]/sm05338
N55e11 has visible | dominant phenotype, enhanceable by sm[+]/smKG03875
N55e11 has visible | dominant phenotype, enhanceable by orb2[+]/orb2BG02373
N55e11 has visible | dominant phenotype, enhanceable by msi[+]/msi1
N55e11 has visible | dominant phenotype, enhanceable by msi[+]/msi2
N55e11 has visible | dominant phenotype, enhanceable by RpL15[+]/RpL1572
N55e11, RpL15[+]/RpL1572 has visible | dominant phenotype, enhanceable by Su(var)2051
Df(1)N-8/N55e11 has visible phenotype, enhanceable by Hr3k09242
Df(1)N-8/N55e11 has visible phenotype, enhanceable by eIF4A162-3
Df(1)N-8/N55e11 has visible phenotype, enhanceable by ptcE227-2
Df(1)N-8/N55e11 has visible phenotype, enhanceable by ptcE291-6
Df(1)N-8/N55e11 has visible phenotype, enhanceable by ptcE470-3
Df(1)N-8/N55e11 has visible phenotype, enhanceable by ptcX234-1
Df(1)N-8/N55e11 has visible phenotype, enhanceable by ptcX253-4
Df(1)N-8/N55e11 has visible phenotype, enhanceable by AcslE305-3
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
N55e11 has size defective | dominant | adult stage | temperature conditional phenotype, suppressible | partially by XxyltΔcds/XxyltΔcds
N55e11 has size defective | dominant | adult stage | temperature conditional phenotype, suppressible | partially by shamsΔ34/shams[+]
N55e11 has size defective | dominant | adult stage | temperature conditional phenotype, suppressible | partially by shamsΔ34/shamsΔ34
N55e11 has size defective | dominant | adult stage | temperature conditional phenotype, suppressible | partially by shamsΔ34/shams[+], XxyltΔcds/XxyltΔcds
N55e11 has visible | adult stage phenotype, suppressible | partially by trr[+]/trrK662X
N55e11 has visible | dominant phenotype, suppressible by lidk06801/lid[+]
N55e11 has visible | dominant phenotype, suppressible by Sin3A[+]/Sin3A08269
N55e11 has visible phenotype, suppressible by GPHRc06331/CG8090[+]
N55e11 has visible phenotype, suppressible by f06222f06222/f06222[+]
N55e11 has visible | dominant phenotype, suppressible by spen[+]/spenXFM911
N55e11 has visible | dominant phenotype, suppressible by spen[+]/spenAH393
N55e11 has visible | dominant phenotype, suppressible | partially by Mycdm-1/dm[+]
N55e11 has visible | dominant phenotype, suppressible by DlM1/Dl[+]
N55e11 has visible | dominant phenotype, suppressible by Dsor1Su1
N55e11 has visible | dominant phenotype, suppressible by wgS107
N55e11 has visible phenotype, suppressible by HC57
N55e11 has visible phenotype, suppressible by HC73
N55e11 has visible phenotype, suppressible by vnC221
N55e11 has visible phenotype, suppressible by E(Egfr)B56B56
N55e11 has visible phenotype, suppressible by E(Egfr)C12C12
N55e11 has visible phenotype, suppressible by E(Egfr)C22C22
N55e11 has visible phenotype, suppressible by HC21
N55e11 has visible phenotype, suppressible by HC24
NOT suppressed by
Statement
Reference
N55e11 has size defective | dominant | adult stage | temperature conditional phenotype, non-suppressible by Xxylt[+]/XxyltΔcds
N55e11 has size defective | dominant | adult stage | temperature conditional phenotype, non-suppressible by Xxyltgt-wt.Tag:V5, XxyltΔcds/XxyltΔcds
N55e11 has visible | adult stage phenotype, non-suppressible by Neurl447b-2
N55e11 has visible | adult stage phenotype, non-suppressible by Lrrk[+]/Lrrke03680
Enhancer of
Statement
Reference
N+/N55e11 is an enhancer of visible | adult stage phenotype of Sirt12A-7-11
N[+]/N55e11 is an enhancer of visible phenotype of Scer\GAL4A9, uifasterisk.UAS
N[+]/N55e11 is an enhancer of visible | recessive phenotype of rumi44
aosΔ7, argos[+], N[+], N55e11 is an enhancer of planar polarity defective phenotype of Pcyt116919
N[+]/N55e11 is an enhancer of visible | somatic clone phenotype of emc1
NOT Enhancer of
Statement
Reference
N[+]/N55e11 is a non-enhancer of visible phenotype of pydtam/pydex147
N[+]/N55e11 is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
N55e11 is a non-enhancer of cell polarity defective phenotype of pkpk.sev
argos[+], aosW11, N[+], N55e11 is a non-enhancer of planar polarity defective phenotype of Pcyt116919
Suppressor of
Statement
Reference
N+/N55e11 is a suppressor | partially of visible | heat sensitive phenotype of Dcr-2UAS.cDa, EogtGD5084, Scer\GAL4en.PU
N55e11 is a suppressor of visible | heat sensitive phenotype of HC2.hs
N[+]/N55e11 is a suppressor of visible | dominant phenotype of DlM1
N55e11 is a suppressor of visible phenotype of aopA141
N55e11 is a suppressor of visible phenotype of aoppok-x8
NOT Suppressor of
Statement
Reference
N[+]/N55e11 is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
N55e11 is a non-suppressor of cell polarity defective phenotype of pkpk.sev
N[+]/N55e11 is a non-suppressor of visible phenotype of Scer\GAL4sca-537.4, dbrEP456
N[+]/N55e11 is a non-suppressor of visible phenotype of Scer\GAL4sca-537.4, tweEP613
N[+]/N55e11 is a non-suppressor of visible phenotype of Scer\GAL4sca-537.4, touEP622
N[+]/N55e11 is a non-suppressor of visible phenotype of Scer\GAL4sca-537.4, aopEP598
N[+]/N55e11 is a non-suppressor of visible phenotype of Scer\GAL4sca-537.4, fafEP381
N[+]/N55e11 is a non-suppressor of visible phenotype of Scer\GAL4sca-537.4, grpEP587
N[+]/N55e11 is a non-suppressor of visible phenotype of Scer\GAL4sca-537.4, elBEP965
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
N55e11 has wing vein phenotype, enhanceable by Sirt1[+]/Sirt12A-7-11
N55e11 has wing phenotype, enhanceable by p53[+]/p5311-1B-1
N55e11 has wing phenotype, enhanceable by p535A-1-4/p53[+]
N55e11 has wing phenotype, enhanceable by p53[+]/p53-ns
N55e11 has wing margin phenotype, enhanceable by dpn[+]/dpn1
N55e11 has wing margin phenotype, enhanceable by dpn[+]/dpn6
N55e11 has wing phenotype, enhanceable by talUAS.cPa/Scer\GAL4dpp.blk1
N55e11 has wing phenotype, enhanceable by Df(2L)ED7819/α4GT11
N55e11 has wing phenotype, enhanceable by sca[+]/scad09400
N55e11 has wing phenotype, enhanceable by klud00059/klu[+]
N55e11 has wing phenotype, enhanceable by lark[+]/lark1
N55e11 has wing phenotype, enhanceable by sm[+]/sm1
N55e11 has wing phenotype, enhanceable by sm[+]/sm05338
N55e11 has wing phenotype, enhanceable by sm[+]/smKG03875
N55e11 has wing phenotype, enhanceable by orb2[+]/orb2BG02373
N55e11 has wing phenotype, enhanceable by msi[+]/msi1
N55e11 has wing phenotype, enhanceable by msi[+]/msi2
N55e11 has wing margin phenotype, enhanceable by RpL15[+]/RpL1572
N55e11, RpL15[+]/RpL1572 has wing margin phenotype, enhanceable by Su(var)2051
N55e11 has wing phenotype, enhanceable by Cct1[+]/Pcyt1179
N55e11 has wing phenotype, enhanceable by Pcyt1299/Cct1[+]
N55e11 has wing phenotype, enhanceable by EgfrE3/Egfr[+]
N55e11 has wing phenotype, enhanceable by Pcyt116919/Cct1[+]
N55e11 has wing phenotype, enhanceable by ebiE4
Df(1)N-8/N55e11 has scutum & macrochaeta | ectopic phenotype, enhanceable by AcslE305-3
Df(1)N-8/N55e11 has scutum & macrochaeta | ectopic phenotype, enhanceable by Hr3k09242
Df(1)N-8/N55e11 has scutum & macrochaeta | ectopic phenotype, enhanceable by eIF4A162-3
Df(1)N-8/N55e11 has scutum & macrochaeta | ectopic phenotype, enhanceable by ptcE227-2
Df(1)N-8/N55e11 has scutum & macrochaeta | ectopic phenotype, enhanceable by ptcE291-6
Df(1)N-8/N55e11 has scutum & macrochaeta | ectopic phenotype, enhanceable by ptcE470-3
Df(1)N-8/N55e11 has scutum & macrochaeta | ectopic phenotype, enhanceable by ptcX234-1
Df(1)N-8/N55e11 has scutum & macrochaeta | ectopic phenotype, enhanceable by ptcX253-4
N55e11 has phenotype, enhanceable by kuz1405Rev11
N55e11 has phenotype, enhanceable by kuz1405Rev4
N55e11 has wing phenotype, enhanceable by hrgP1
N55e11 has wing vein phenotype, enhanceable by hrgP1
NOT Enhanced by
Statement
Reference
N55e11 has wing phenotype, non-enhanceable by p535A-1-4/Dp(3;3)M95A+13
N55e11 has wing phenotype, non-enhanceable by Scer\GAL4dpp.blk1/tal1-4FS.UAS
N55e11 has wing phenotype, non-enhanceable by Egfr[+]/Egfrtop-18A
N55e11 has wing phenotype, non-enhanceable by aosΔ7/argos[+]
Suppressed by
Statement
Reference
N55e11 has wing margin | temperature conditional phenotype, suppressible | partially by XxyltΔcds/XxyltΔcds
N55e11 has wing vein | temperature conditional phenotype, suppressible | partially by XxyltΔcds/XxyltΔcds
N55e11 has wing margin | temperature conditional phenotype, suppressible | partially by shamsΔ34/shams[+]
N55e11 has wing vein | temperature conditional phenotype, suppressible | partially by shamsΔ34/shams[+]
N55e11 has wing margin | temperature conditional phenotype, suppressible | partially by shamsΔ34/shamsΔ34
N55e11 has wing vein | temperature conditional phenotype, suppressible | partially by shamsΔ34/shamsΔ34
N55e11 has wing margin | temperature conditional phenotype, suppressible | partially by shamsΔ34/shams[+], XxyltΔcds/XxyltΔcds
N55e11 has wing vein | temperature conditional phenotype, suppressible | partially by shamsΔ34/shams[+], XxyltΔcds/XxyltΔcds
N55e11 has wing margin phenotype, suppressible | partially by trr[+]/trrK662X
N55e11 has wing vein phenotype, suppressible by shamse01256/shamse01256
N55e11 has wing vein phenotype, suppressible by lidk06801/lid[+]
N55e11 has wing vein phenotype, suppressible by Sin3A[+]/Sin3A08269
N55e11 has wing phenotype, suppressible by GPHRc06331/CG8090[+]
N55e11 has wing phenotype, suppressible by f06222f06222/f06222[+]
N55e11 has wing phenotype, suppressible by spen[+]/spenXFM911
N55e11 has wing phenotype, suppressible by spen[+]/spenAH393
N55e11 has chaeta | ectopic phenotype, suppressible | partially by Mycdm-1/dm[+]
N55e11 has wing phenotype, suppressible by DlM1/Dl[+]
N55e11 has wing vein phenotype, suppressible by DlM1/Dl[+]
N55e11 has wing margin phenotype, suppressible by Dsor1Su1
N55e11 has wing phenotype, suppressible by HC57
N55e11 has wing phenotype, suppressible by HC73
N55e11 has wing phenotype, suppressible by vnC221
N55e11 has wing phenotype, suppressible by E(Egfr)B56B56
N55e11 has wing phenotype, suppressible by E(Egfr)C12C12
N55e11 has wing phenotype, suppressible by E(Egfr)C22C22
N55e11 has wing phenotype, suppressible by HC21
N55e11 has wing phenotype, suppressible by HC24
NOT suppressed by
Statement
Reference
N55e11 has wing margin | temperature conditional phenotype, non-suppressible by Xxylt[+]/XxyltΔcds
N55e11 has wing vein | temperature conditional phenotype, non-suppressible by Xxylt[+]/XxyltΔcds
N55e11 has wing margin | temperature conditional phenotype, non-suppressible by Xxyltgt-wt.Tag:V5, XxyltΔcds/XxyltΔcds
N55e11 has wing vein | temperature conditional phenotype, non-suppressible by Xxyltgt-wt.Tag:V5, XxyltΔcds/XxyltΔcds
N55e11 has wing vein | adult stage phenotype, non-suppressible by Neurl447b-2
N55e11 has wing vein | adult stage phenotype, non-suppressible by Lrrk[+]/Lrrke03680
N55e11 has wing phenotype, non-suppressible by Scer\GAL4dpp.blk1/tal1-4FS.UAS
Enhancer of
Statement
Reference
N[+]/N55e11 is an enhancer of wing vein phenotype of Scer\GAL4A9, uifasterisk.UAS
N[+]/N55e11 is an enhancer of microchaeta phenotype of rumi44
N[+]/N55e11 is an enhancer of mesothoracic tergum & chaeta | supernumerary phenotype of lqfARI
aosΔ7, argos[+], N[+], N55e11 is an enhancer of eye photoreceptor cell phenotype of Pcyt116919
aosΔ7, argos[+], N[+], N55e11 is an enhancer of ommatidium phenotype of Pcyt116919
N[+]/N55e11 is an enhancer of eye phenotype of Pcyt116919
N55e11 is an enhancer of ommatidium phenotype of Gp150k11120b
N[+]/N55e11 is an enhancer of wing vein | somatic clone phenotype of emc1
N55e11 is an enhancer of phenotype of Brd1
N55e11 is an enhancer of phenotype of Brd3
N55e11 is an enhancer of wing phenotype of hrgP1
NOT Enhancer of
Statement
Reference
N+/N55e11 is a non-enhancer of type II neuroblast | larval stage phenotype of dpn7
N[+]/N55e11 is a non-enhancer of wing phenotype of pydtam/pydex147
N[+]/N55e11 is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
N55e11 is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, pksple.UAS
N55e11 is a non-enhancer of ommatidium phenotype of pkpk.sev
N[+]/N55e11 is a non-enhancer of photoreceptor cell R8 | supernumerary phenotype of ed4.12
argos[+], aosW11, N[+], N55e11 is a non-enhancer of eye photoreceptor cell phenotype of Pcyt116919
argos[+], aosW11, N[+], N55e11 is a non-enhancer of ommatidium phenotype of Pcyt116919
Suppressor of
Statement
Reference
N[+]/N55e11 is a suppressor of germarium cap cell | supernumerary phenotype of pydex147
N[+]/N55e11 is a suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa
N55e11 is a suppressor of wing vein | ectopic | heat sensitive phenotype of HC2.hs
N55e11 is a suppressor of wing | heat sensitive phenotype of HC2.hs
N[+]/N55e11 is a suppressor of wing phenotype of DlM1
N[+]/N55e11 is a suppressor of wing vein phenotype of DlM1
N55e11 is a suppressor of ommatidium phenotype of aopA141
N55e11 is a suppressor of ommatidium phenotype of aoppok-x8
NOT Suppressor of
Statement
Reference
N+/N55e11 is a non-suppressor of type II neuroblast | larval stage phenotype of dpn7
N[+]/N55e11 is a non-suppressor of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
N55e11 is a non-suppressor of ommatidium phenotype of pkpk.sev
N55e11 is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, VangUAS.cWa
N55e11 is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, pksple.UAS
N[+]/N55e11 is a non-suppressor of photoreceptor cell R8 | supernumerary phenotype of ed4.12
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
N55e11 hemizygous males bearing one copy of Ngt-16-20 show wing vein loss, which is not suppressed by the expression of XxyltUAS.Tag:HA under the control of Scer\GAL4nub.PU. The wing margin loss and wing vein thickening observed in N55e11 hemizygous males are partially suppressed by XxyltΔcds homozygosity; these defects are also partially suppressed by shamsΔ34 heterozygosity and (more efficiently) homozygosity; suppression by the combination of XxyltΔcds homozygosity and shamsΔ34 heterozygosity is more efficient than by either single mutant.
N55e11 heterozygosity suppresses the increased number and size of circulating crystal cells observed in DnaJ-1A/DnaJ-1C transheterozygous or MlfΔC1 homozygous third instar larvae.
N55e11 heterozygous adults also expressing Rbfox1dsRNA.Scer\UAS under the control of Scer\GAL4sca-109-68 display an enhancement of the supernumerary thoracic sensory bristle phenotype, even leading to ectopic thoracic bristles, as compared to either N55e11 heterozygotes or individuals only expressing Rbfox1dsRNA.Scer\UAS under the control of Scer\GAL4sca-109-68.
The formation of extra scutellar bristles observed in either Sirt12A-7-11/Sirt12A-7-11 or N55e11/+ single mutants is strongly enhanced in N55e11/+;Sirt12A-7-11/Sirt12A-7-11 double mutants, which on average have around seven scutellar bristles (instead of the four normally found in wild-type flies). The severity (width) of the vein deltas phenotype characteristic for N55e11 heterozygotes is increased by hetero- or (more strongly) homozygosity of Sirt12A-7-11.
Df(2R)mir-7-Δ1/Df(2R)exu1 suppresses wing notching seen in N55e11/+ flies. N55e11/+ suppresses the severity of decreases in wing size seen in Df(2R)mir-7-Δ1/Df(2R)exu1 flies.
The vein thickening and ectopic veins phenotype characteristic for N55e11 mutant adults is not modified by expression of either Neurl4EY12221 or HERC2G17171 under the control of Scer\GAL4dpp.PU in the mutant background or by combination with Neurl447b-2 or Lrrke03680.
insbΔ1/Df(2R)BSC406 suppresses the bristle density phenotype seen in N55e11/+ mutant flies.
Addition of N55e11/+ to individuals expressing p53UAS.DΔNp53 under the control of Scer\GAL4sd.PU exacerbates the decrease in wing disc size, reduces wing pouch protruding overgrowths and results in much smaller adult wings compared to controls.
Expression of shgKK103334 under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 suppresses the retention of N55e11 mutant germline stem cells seen in females at two weeks after clone induction.
dpn1/+ enhances the wing notching phenotype seen in N55e11/+ flies (78% of flies have wing nicks). dpn6/+ enhances the wing notching phenotype seen in N55e11/+ flies (97% of flies have wing nicks).
The wing-notching phenotype characteristic for N55e11/+ adult flies is partially suppressed by combination with a single copy of trrK662X.
The wing blistering phenotype seen in the posterior compartment of wings in flies expressing EogtGD5084 under the control of Scer\GAL4en.PU in the presence of Dcr-2Scer\UAS.cDa is dominantly partially suppressed if the flies are also heterozygous for N55e11.
The wing notching seen in N55e11/+ females is completely suppressed by expression of P{UAS-mCh.mir-13b.sponge.T} under the control of Scer\GAL4ptc-559.1. The wing notching seen in N55e11/+ females is partially suppressed by expression of either P{UAS-mCh.mir-2b.sponge.T}, mir-2csponge.Scer\UAS.T:Disc\RFP-mCherry or mir-13asponge.Scer\UAS.T:Disc\RFP-mCherry under the control of Scer\GAL4ptc-559.1. The wing notching seen in N55e11/+ females is not suppressed by expression of either P{UAS-mCh.mir-6.sponge.T}, mir-7sponge.Scer\UAS.T:Disc\RFP-mCherry or Disc\RFPmCh.Scer\UAS.SCRAMBLE.sponge under the control of Scer\GAL4ptc-559.1.
Introducing N55e11/+ into the Scer\GAL4pnr-MD237, Usp12-46GD12106 background results in a partial restoration of normal phenotype because the cell fate transformation into socket cells is seldom observed, although lateral inhibition problems as well as malformation of the notum are still obvious.
N55e11/+ strongly enhances the Scer\GAL4hs.2sev>hbsVDRC.cUa-induced eye phenotype. Specifically, N55e11/+, Scer\GAL4hs.2sev>hbsVDRC.cUa eyes display a marked increase in R3-R3 symmetrical clusters compared with Scer\GAL4hs.2sev>hbsVDRC.cUa eyes. N55e11/+ enhances the Df(2R)hbsj5/Df(2R)ED2423-associated notal microchaeta-loss phenotype.
The premature loss of neuroblasts seen in N55e11 type II neuroblast clones is completely suppressed by expression of kluScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act5C.PP. Supernumerary neuroblasts are not induced in these clones.
The decrease in the number of type II neuroblasts in the brain that is seen in dpn7/+ larvae is unaffected if the animals are also heterozygous for N55e11.
100% of N55e11/+; pydex147/Df(3R)p-XT103 flies display more than four dorsocentral macrochaetae. The broader wings observed in pydex147/pydtam flies are not enhanced in a N55e11/+ background. N55e11/+ suppresses the increased ovarian cap cell numbers observed in pydex147/+ mutants. 100% of N55e11/+; pydtam/pydC5 flies display more than four dorsocentral macrochaetae.
N55e11/+ suppresses the ommatidial over-rotation phenotype which is caused by expression of nmoScer\UAS.cUa under the control of Scer\GAL4hs.2sev.
Expression of talScer\UAS.cPa by Scer\GAL4dpp.blk1 in N55e11 heterozygotes strongly enhances the expansion of L3 veins with complete penetrance. Expression of tal1-4FS.Scer\UAS by Scer\GAL4dpp.blk1 in N55e11 heterozygotes does not modify L3 wing vein formation. Expression of talScer\UAS.cPa by Scer\GAL4dpp.blk1 enhances the wing-notching phenotype found in N55e11 heterozygotes. Expression of talORF1.Scer\UAS by Scer\GAL4dpp.blk1 enhances the wing-notching phenotype found in N55e11 heterozygotes. Expression of tal1-4FS.Scer\UAS by Scer\GAL4dpp.blk1 does not affect the wing-notching phenotype found in N55e11 heterozygotes.
The wing nicking phenotype seen in N55e11/+ flies is enhanced by α4GT11/Df(2L)ED7819.
The thickening of the wing veins that is seen in N55e11/+ flies is suppressed by lidk06801/+ or Sin3A08269/+.
Clones of cells generated at 24-48 or 48-72 hrs AEL which are mutant for N55e11 and express armS10.Scer\UAS.T:Hsap\MYC via Scer\GAL4αTub84B.PL (generated using the MARCM system) give rise to tightly packed spheres with large numbers of cells and abnormal polarity in the wing disc. Similar clones generated after 72hrs appear scattered through the tissue, lose basal contact and exhibit a variety of organizations. The over-proliferation defect of clones of cells mutant for N55e11 and expressing armS10.Scer\UAS.T:Hsap\MYC Scer\GAL4αTub84B.PL (generated using the MARCM system) are rescued by co-expression of Nintra.Scer\UAS.T:Avic\GFP-EGFP,T:Mmus\Cd8a. Clones of cells which are mutant for N55e11 and express armS10.Scer\UAS.T:Hsap\MYC via Scer\GAL4dpp.PU are relatively few but contain a relatively large number of cells. Clones of cells mutant for N55e11 and expressing armS10.Scer\UAS.T:Hsap\MYC via Scer\GAL4dpp.PU are smaller and more frequent when Nintra.Scer\UAS.T:Avic\GFP-EGFP,T:Mmus\Cd8a or NFLN.Scer\UAS is coexpressed.
rumi44 hemizygotes raised at 18oC and also carrying N55e11/+ show loss of microchaetae.
Expression of amxScer\UAS.cMa under the control of Scer\GAL4arm.PU does not suppress the neurogenic cuticle phenotypes seen in male stage 8 embryos derived from heterozygous N55e11 mutant females.
The distal wing notching shown by N55e11/+ flies is enhanced by scad09400 or klud00059. The distal wing notching shown by N55e11/+ flies is dominantly suppressed to wild type at high penetrance by CG8090c06331 or f06222f06222. One copy of msi2, msi1, orb2BG02373, smKG03875, sm05338, sm1 or lark1 enhances the N55e11/+ wing nicking phenotype. One copy of spenXFM911 or spenAH393 suppresses the N55e11/+ wing nicking phenotype. N55e11/+ has little if any effect on the mutant eye phenotype of armS56F.GMR or armS44Y.GMR flies.
The ectopic bristle phenotype seen in N55e11/+ females is partially suppressed if they are also heterozygous for dm1.
Bre1ΔRING.Scer\UAS, under the regulation of Scer\GAL4Bx-MS1096 enhances the phenotype of N55e11/+ resulting in an increase in the thickness of wing veins and additional vein material. In the case of N55e11/+ an increase in wing notching is also found. The vein thickening and additional vein material phenotype of flies expressing Bre1Scer\UAS.fl, under the regulation of Scer\GAL4Bx-MS1096 is enhanced in N55e11 heterozygotes.
Unlike either heterozygote, tan2/+ N55e11/+ mutants display a strong reduction in occellar bristle number. The effect of bristle number reduction, as seen in the N55e11/+; tan2/+ transheterozygotes can be alleviated by providing a single copy of tant7.
RpL1572/+ slightly enhances the weak wing margin phenotype of N55e11/+. The effect of RpL1572 on N55e11 is further enhanced if the flies also carry Su(var)2051.
40% of N55e11 ; lqfARI double heterozygotes have extra notal bristles.
N55e11/+ ; ed1X5/edslH8 adults show an almost complete absence of microchaetae on the notum.
The ed4.12 R8 cell twinning phenotype is not altered by N55e11/+.
The wing notching phenotype seen in N55e11/+ flies is dominantly enhanced by Cct1 alleles. This enhancement is stronger with the null alleles Cct1179 and Cct1299 than with the weaker hypomorphic Cct116919 allele. The phenotype is most greatly enhanced in flies that are heterozygous for both EgfrE3 and N55e11, with over 80% of these flies showing the notched phenotype compared to less than 10% in N55e11/+ single mutants. The notch phenotype is not enhanced in argosΔ7/+ or Egfrtop-18A/+ mutants. N55e11/+; Cct116919/+, argosΔ7/+ triple heterozygotes show an enhancement in the defective eye phenotype (loss of photoreceptor cells, defects in ommatidial polarity and chirality and a partial loss of the ventral eye) seen in Cct116919 mutants. This phenotype is not significantly enhanced in Cct116919/+, argosW11/+, N55e11/+ triple heterozygotes. The Cct116919 homozygous phenotype is strongly enhanced in N55e11/+ background mutants causing severely reduced eyes.
The addition of N55e11/+ to Gp150P8/Gp150k11120b animals increases the proportion of mutant ommatidia from 19.2% to 42.3%. The addition of N55e11/+ to Gp150k11120b/+ animals increases the proportion of mutant ommatidia from 0.19% to 0.65%.
The addition of btl::EgfrScer\UAS.T:λ\cI-DD has no effect on the N55e11 Malpighian tubule phenotype.
The wing notching phenotype of N55e11 animals is enhanced by the addition of ebiE4.
Has no effect on the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).
frcNP0297 in double heterozygous combination with N55e11 results in duplications of the anterior scutellar bristles.
Clones of N55e11/N55e11; emc1/Df(3L)emc-E12 cells in the wing have extremely poor viability. The width of wing veins formed by clones of homozygous emc1 cells is increased if the flies are also heterozygous for N55e11.
The addition of N55e11 to Su(H)Scer\UAS.cKa, Su(H)ΔH.Scer\UAS or Su(H)Scer\UAS.T:SV40\nls2 flies when driven by Scer\GAL4dpp.blk1 or Scer\GAL4ptc-559.1 flies leads to a strong enhancement of the wing nicking phenotype.
The wing veins and margin are normal in N55e11/+ ; DlM1/+ double heterozygotes.
The wing margin defects of heterozygotes are suppressed by Dsor1Su1.
Heterozygotes of Df(1)N-8 or N55e11 with Abl1, NrtM54 or In(3L)std11 show defects in eye development leading to rough eyes with high penetrance.
Mutation enhances the ectopic scutellar bristle phenotype seen from Scer\GAL4455.2-mediated expression of l(1)scScer\UAS.cHa. Mutations of eIF-4a, ptc, l(2)44DEa and Hr46 enhance the ectopic notum bristle phenotype of N55e11/Df(1)N-8 transheterozygotes.
The number of bristles is not altered if N55e11/+ flies are also heterozygous for Df(3R)Dl-FX3, however the number of bristles is restored to wild-type in N55e11 ; wgS107 double heterozygotes.
The cuticle defect of homozygous embryos is not rescued by bibScer\UAS.cDa expressed under the control of Scer\GAL4h-1J3.
The N55e11/+ phenotype is enhanced by kuz1405Rev4/kuz1405Rev11.
N55e11/+; Df(2R)vg-B double heterozygotes show severe notching of the wing. N55e11/+; vgs2/vgs2 flies show increased cell death in the wing, and many ectopic bristles are found on the wing surface, especially on vein L4. N55e11/+; hi22/+ flies have severe notching of the wings. N55e11/+; Df(2R)vg-B/+ hi22/+ flies are viable and have small wings.
The N55e11/+ notched wing phenotype is increased when numbScer\UAS.cWa expression is driven by Scer\GAL4ptc-559.1 in these flies.
The wing phenotype is synergistically enhanced in N55e11/+ ; hrgP1/hrgP1 flies; all flies have notched wings, and the third and fifth wing veins are thicker than in N55e11/+ single mutants.
N55e11/+ Egfrt1/Egfrf11 flies and N55e11/+ EgfrE3/+ flies show a simple additive phenotype.
Xenogenetic Interactions
Statement
Reference
The vein thickening and ectopic veins phenotype characteristic for N55e11 mutant adults is not modified by expression of Hsap\LRRK2Scer\UAS.cVa under the control of Scer\GAL4dpp.PU in the mutant background.
Expression of Hsap\PTOV1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4nub.PU enhances the wing notching phenotype seen in N55e11 mutant flies. There is a significant increase in the number of notches per wing compared with N55e11 alone.
One copy of N55e11 enhances the wing notching and ectopic bristle phenotypes seen when Mmus\Dlk1SM.Scer\UAS is expressed under the control of Scer\GAL4ptc-559.1 at 25[o]C. Neither the decrease in number nor the increase in size of the cells between the L3 and L4 wing veins shows any enhancement. One copy of N55e11 enhances the wing notching and ectopic bristle phenotypes seen when Mmus\Dlk1M.Scer\UAS is expressed under the control of Scer\GAL4ptc-559.1 at 25[o]C.
Complementation and Rescue Data
Not rescued by
Comments
Expression of NT:Disc\RFP-mCherry fully rescues N55e11 mutant phenotypes. Expression of NT:Avic\GFP,T:Disc\RFP-mCherry fully rescues N55e11 mutant phenotypes.
Scer\GAL4arm.T:Hsim\VP16-mediated expression of N3intron.Scer\UAS rescues the CNS and PNS differentiation defects.
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Mohler, May 1955.
Comments
Comments
Cell autonomous in mosaic analysis carried out in the last stages of the formation of the adult sensory organs.
Behaves as does Df(1)N-8 in interaction tests with wg alleles.
No interaction with P{sev-svp1} or P{sev-svp2} exists.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (15)
Reported As
Symbol Synonym
N55e11
(Bala Tannan et al., 2018, Li et al., 2018, Pandey et al., 2018, Petruccelli et al., 2018, Corson et al., 2017, Miller et al., 2017, Shukla et al., 2017, Horvath et al., 2016, Slaninova et al., 2016, Aparicio et al., 2015, Beehler-Evans and Micchelli, 2015, Imai et al., 2015, Jia et al., 2015, Alaña et al., 2014, Coumailleau and Schweisguth, 2014, Couturier et al., 2014, Haltom et al., 2014, Simón et al., 2014, Small et al., 2014, Tseng et al., 2014, Chang et al., 2013, Guichard et al., 2013, Kanda et al., 2013, Langen et al., 2013, Lee et al., 2013, Lee et al., 2013, Boukhatmi et al., 2012, Couturier et al., 2012, de Navascués et al., 2012, Moretti et al., 2012, Singh and Mlodzik, 2012, Weng et al., 2012, Xie et al., 2012, Yamakawa et al., 2012, Banks et al., 2011, Djiane et al., 2011, Eliazer et al., 2011, Endo et al., 2011, Hwang and Rulifson, 2011, Leonardi et al., 2011, Mirkovic et al., 2011, Pi et al., 2011, San-Juán and Baonza, 2011, Tsubota et al., 2011, Zhang et al., 2011, Das et al., 2010, Djiane and Mlodzik, 2010, Hamel et al., 2010, Kugler and Nagel, 2010, Levine et al., 2010, Mathur et al., 2010, Richardson and Pichaud, 2010, Boyle and Berg, 2009, Moshkin et al., 2009, Sanders et al., 2009, Udolph et al., 2009, Vied and Kalderon, 2009, Acar et al., 2008, Bray et al., 2008, Michellod and Randsholt, 2008, Assa-Kunik et al., 2007, Kankel et al., 2007, Orian et al., 2007, Sasamura et al., 2007, Bayraktar et al., 2006, Beckett and Baylies, 2006, Jordan et al., 2006, Joshi et al., 2006, Ward et al., 2006, Almeida and Bray, 2005, Hayward et al., 2005, Brodu et al., 2004, Kamimura et al., 2004, Kamimura et al., 2004, Rath et al., 2002)
Notch55ell
notch55e11
Name Synonyms
Secondary FlyBase IDs
    References (247)