A Database of Drosophila Genes & Genomes

FB2008_07, released August 8, 2008
 

Allele Dmel\N55e11

General Information
SymbolDmel\N55e11SpeciesD. melanogaster
NameFlyBase IDFBal0012701
Feature typealleleCreated / Updated2006-05-15/2006-05-15
Associated geneDmel\N
Allele classamorph, loss of function, hypomorph
Mutagenspontaneous
hide Nature of the Allele
Allele class
amorph
(Campos-Ortega, 1983, de la Concha et al., 1988, Heitzler and Simpson, 1991, Ruohola et al., 1991, de Celis et al., 1991, Mari-Beffa et al., 1991, de Celis et al., 1993, Couso and Martinez Arias, 1994, Rulifson and Blair, 1995, Heitzler et al., 1996, Sun and Deng, 2005)
loss of function
(Lehmann et al., 1983, de Celis and Garcia-Bellido, 1994, de Celis et al., 1991, Abu-Issa and Cavicchi, 1996, Long et al., 1996, Murata et al., 1996, Seugnet et al., 1997, de Celis et al., 1997, Brennan et al., 1997, Torres et al., 2003, Weber et al., 2003, Kamimura et al., 2004, Kamimura et al., 2004)
hypomorph
(Tian et al., 2004)
Mutagen
spontaneous
 
Mapped Features and Mutations
Type
Symbol & Location
Additional Notes
References
 
 
 
 
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      Progenitor genotype
      Nature of the lesion
      Statement
      Reference
      Lesion in Notch caused by a 3.5 kb insertion in the vicinity of coordinate -26, '+' values to the right, '-' values to the left (Kidd, Lockett and Young, 1983).
       
      Insertion of a copia-like element at coordinate -26kb (coordinates according to FBrf0045027 and FBrf0039003).
      (Kelley et al., 1987)
      Insertion in 5' coding region: premature termination of transcripts.
      (Heitzler and Simpson, 1991)
      Insertion upstream of EGF repeats.
      (Couso and Martinez Arias, 1994)
      3.5kb insertion in the 5' coding region that causes premature termination of transcripts.
      (Rulifson and Blair, 1995)
      An insertion in the 5' coding region and premature termination of transcripts.
      (Heitzler et al., 1996)
      Insertion closely associated with the first exon.
      (Brennan et al., 1997)
      Assay mode
      Caused by insertion
      ?{}N55e11
      (Takatsu et al., 2000, Rauskolb et al., 1999, Brennan et al., 1997, Kelley et al., 1987, Torres et al., 2003, Jenny et al., 2003, Lindsley and Zimm, 1992)
      Cytology
      Polytene chromosomes normal (Welshons).
       
      hide Phenotypic Data
      hide Phenotypic Class
      lethal (with Nl1N-ts1)
      (Micchelli and Perrimon, 2006)
      lethal | recessive
      (Long et al., 1996)
      lethal | embryonic stage | neurogenic | recessive
      (Lehmann et al., 1983)
      visible
      (Price et al., 1997, Vassin et al., 1985)
      visible (with Df(1)N-8)
      (Rottgen et al., 1998)
      visible | recessive | conditional - heat sensitive
      (Bishop et al., 1999)
      visible | recessive | somatic clone
      (Zeng et al., 1998)
      visible | dominant
      (Sotillos et al., 1997, Frise et al., 1996, Schulze et al., 2005, de Celis and Bray, 2000, Roch et al., 1998, Nagaraj et al., 1999, Glise et al., 2002, Abu-Issa and Cavicchi, 1996, Murata et al., 1996, Long et al., 1996, Kamimura et al., 2004)
      visible | dominant | neurogenic
      (Brennan et al., 1997)
      visible | somatic clone
      (Rauskolb and Irvine, 1999)
      neuroanatomy defective
      (Le Gall and Giniger, 2004)
      hide Phenotype Manifest In
      wing (with Df(3L)Ar14-8)
      (Weber et al., 2003)
      abdominal ventral multidendritic neuron | ectopic (with Nl1N-ts1)
      (Orgogozo et al., 2002)
      external sensory organ precursor cell | ectopic (with Nl1N-ts1)
      (Orgogozo et al., 2002)
      wing
      (Weber et al., 2003, Sotillos et al., 1997, Frise et al., 1996, Tsuda et al., 2002, Price et al., 1997, Vassin et al., 1985, de Celis and Bray, 2000, de Celis et al., 1996, Abu-Issa and Cavicchi, 1996, Murata et al., 1996, de Celis and Garcia-Bellido, 1994)
      leg | conditional - heat sensitive
      (Bishop et al., 1999)
      prothoracic tibial apical bristle | conditional - heat sensitive
      (Bishop et al., 1999)
      mesothoracic tibial apical bristle | conditional - heat sensitive
      (Bishop et al., 1999)
      wing vein
      (Sotillos et al., 1997, Vassin et al., 1985, Sturtevant and Bier, 1995, Roch et al., 1998, Glise et al., 2002, de Celis et al., 1996, Abu-Issa and Cavicchi, 1996, Murata et al., 1996, Crozatier et al., 2003)
      fusion competent cell & visceral mesoderm
      (Stute et al., 2004)
      muscle founder cell & visceral mesoderm
      (Stute et al., 2004)
      external sensory organ | somatic clone
      (Frise et al., 1996)
      Malpighian tubule tip cell
      (Hoch and Jackle, 1998)
      dMP2 neuron | ectopic | germ-line clone
      (Rusconi and Corbin, 1999)
      vMP2 neuron | ectopic | germ-line clone
      (Rusconi and Corbin, 1999)
      RP2 neuron | ectopic | germ-line clone
      (Rusconi and Corbin, 1999)
      neuroblast NB5-2 | germ-line clone
      (Seugnet et al., 1997)
      neuroblast NB7-4 | germ-line clone
      (Seugnet et al., 1997)
      larval central nervous system | germ-line clone
      (Seugnet et al., 1997)
      larval peripheral nervous system | germ-line clone
      (Seugnet et al., 1997)
      dorsal mesothoracic disc | dorsal/ventral compartment boundary | somatic clone
      (Micchelli and Blair, 1999)
      ectoderm
      (Bodmer et al., 1993)
      embryonic nervous system
      (Giebel et al., 1997, Bate et al., 1993)
      larval brain & embryo
      (Giebel et al., 1997)
      ventral nerve cord
      (Giebel et al., 1997)
      epidermis
      (Giebel et al., 1997)
      larval foregut & embryo
      (Giebel et al., 1997)
      larval hindgut & embryo
      (Giebel et al., 1997)
      embryonic/larval tracheal system
      (Giebel et al., 1997)
      larval salivary gland & embryo
      (Giebel et al., 1997)
      adult thoracic sensillum
      (Brennan et al., 1997)
      embryonic hindgut
      (Iwaki and Lengyel, 2002)
      Malpighian tubule primordium | germ-line clone
      (Hoch et al., 1994)
      Malpighian tubule tip cell | germ-line clone
      (Hoch et al., 1994)
      embryonic trachea
      (Llimargas, 1999)
      stomatogastric nervous system primordium
      (Gonzalez-Gaitan and Jaeckle, 1995)
      follicle cell | somatic clone
      (Lopez-Schier and St. Johnston, 2001, Torres et al., 2003)
      centripetally migrating follicle cell | somatic clone
      (Lopez-Schier and St. Johnston, 2001)
      interfollicle cell | somatic clone
      (Lopez-Schier and St. Johnston, 2001)
      polar follicle cell | somatic clone
      (Lopez-Schier and St. Johnston, 2001, Adam and Montell, 2004)
      mitotic cell cycle | somatic clone
      (Lopez-Schier and St. Johnston, 2001)
      wing margin
      (Schulze et al., 2005, Nagaraj et al., 1999, Kamimura et al., 2004)
      ventral thoracic disc
      (zur Lage and Jarman, 1999)
      embryonic/larval somatic muscle
      (Rusconi and Corbin, 1998, Bate et al., 1993)
      embryonic/larval somatic muscle | germ-line clone
      (Rusconi and Corbin, 1998)
      joint | cell autonomous | somatic clone
      (Rauskolb and Irvine, 1999)
      joint | cell non-autonomous | somatic clone
      (Rauskolb and Irvine, 1999)
      leg sensillum | somatic clone
      (Rauskolb and Irvine, 1999)
      leg | somatic clone
      (Rauskolb and Irvine, 1999)
      tibia | somatic clone
      (Rauskolb and Irvine, 1999)
      femur | somatic clone
      (Rauskolb and Irvine, 1999)
      embryonic central nervous system
      (Le Gall and Giniger, 2004, Menne and Klambt, 1994)
      embryonic peripheral nervous system
      (Le Gall and Giniger, 2004)
      egg chamber | somatic clone
      (Grammont and Irvine, 2001, Adam and Montell, 2004)
      polar follicle cell | cell autonomous | somatic clone
      (Grammont and Irvine, 2001)
      interfollicle cell | cell non-autonomous | somatic clone
      (Grammont and Irvine, 2001)
      embryonic epidermis
      (Bate et al., 1993, Doherty et al., 1997, Lehmann et al., 1983)
      embryonic myoblast
      (Bate et al., 1993)
      wing vein L3
      (de Celis and Bray, 2000, Kamimura et al., 2004)
      wing vein L5
      (de Celis and Bray, 2000)
      wing vein L3 | ectopic
      (de Celis and Bray, 2000)
      wing vein L5 | ectopic
      (de Celis and Bray, 2000)
      socket & scutum | somatic clone
      (Zeng et al., 1998)
      macrochaeta & scutum | somatic clone
      (Zeng et al., 1998)
      macrochaeta | somatic clone
      (Zeng et al., 1998)
      sensory mother cell | somatic clone
      (Zeng et al., 1998)
      dorsal mesothoracic disc
      (Nagaraj et al., 1999)
      subperineurial glial cell | somatic clone
      (Udolph et al., 2001)
      neuron | somatic clone | supernumerary
      (Udolph et al., 2001)
      pCC neuron | somatic clone
      (Udolph et al., 2001)
      aCC neuron | somatic clone | supernumerary
      (Udolph et al., 2001)
      wing | distal
      (Glise et al., 2002)
      wing margin bristle
      (Glise et al., 2002)
      sensory mother cell | ectopic
      (de Celis et al., 1996)
      macrochaeta
      (de Celis et al., 1996)
      dorsal double row
      (de Celis et al., 1996)
      ventral double row
      (de Celis et al., 1996)
      segment border muscle | precursor
      (Jagla et al., 1998)
      wing sensillum | ectopic
      (Abu-Issa and Cavicchi, 1996)
      follicle cell & nucleus | somatic clone
      (Deng et al., 2001)
      embryonic/larval dorsal vessel | precursor
      (Jagla et al., 1997)
      support cell of the dorsal bipolar dendritic cell
      (Umesono et al., 2002)
      peripheral glial cell 3 | supernumerary
      (Umesono et al., 2002)
      scolopidial ligament cell | supernumerary
      (Umesono et al., 2002)
      multidendritic neuron
      (Vervoort et al., 1997)
      proventriculus inner layer primordium
      (Fuss et al., 2004)
      proventriculus intermediate layer primordium
      (Fuss et al., 2004)
      proventriculus outer layer primordium
      (Fuss et al., 2004)
      embryonic proventriculus
      (Fuss et al., 2004)
      keyhole structure
      (Fuss et al., 2004)
      wing | dorsal/ventral compartment boundary
      (de Celis and Garcia-Bellido, 1994)
      midline glial cell
      (Menne and Klambt, 1994)
      midline glial cell | ectopic
      (Menne and Klambt, 1994)
      Malpighian tubule
      (Sudarsan et al., 2002)
      Malpighian tubule | germ-line clone
      (Sudarsan et al., 2002)
      procrystal cell
      (Lebestky et al., 2003)
      embryonic/first instar larval cuticle
      (Martinez Arias, 1998)
      dorsal mesothoracic disc | somatic clone
      (Rauskolb et al., 1999)
      sensory mother cell
      (Crozatier et al., 2003)
      germline cyst
      (Torres et al., 2003)
      egg chamber
      (Torres et al., 2003)
      oocyte | anterior posterior gradient
      (Torres et al., 2003)
      polar follicle cell
      (Torres et al., 2003)
      interfollicle cell | anterior
      (Torres et al., 2003)
      anterior scutellar bristle
      (Kamimura et al., 2004)
      posterior scutellar bristle
      (Kamimura et al., 2004)
      adult midgut
      (Ohlstein and Spradling, 2007)
      fusion competent cell
      (Beckett and Baylies, 2006)
      scutum & macrochaeta | ectopic (with Df(1)N-8)
      (Rottgen et al., 1998)
      hide Detailed Description
      Statement
      Reference
      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).
       
      Lethal in combination with Nl1N-ts1 or NAx-tsl at 29oC.
      (Shellenbarger and Mohler, 1975)
      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.
      (Poulson and Lefevre, 1982)
      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.
      (Campos-Ortega, 1983)
      Extreme embryonic neurogenic phenotype.
      (Lehmann et al., 1983)
      Notching of the tips and/or edges of the wing. Veins are frequently broadened at the marginal junctions, forming delta-like thickenings.
      (Vassin et al., 1985)
      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.
      (Brand and Campos-Ortega, 1988)
      Post-transcriptional control of AS-C expression is suppressed, all cells expressing RNA accumulate protein.
      (Cabrera, 1990)
      Neural hyperplasia of cells within a mutant clone. Mutant clones fail to form bristles.
      (Heitzler and Simpson, 1991)
      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.
      (Corbin et al., 1991)
      Increase in SMCs per cluster in embryos lacking the maternal product.
      (Goriely et al., 1991)
      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.
      (de Celis et al., 1991)
      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.
      (Skeath and Carroll, 1992)
      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.
      (Bodmer et al., 1993)
      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.
      (Menne and Klambt, 1994)
      Heterozygotes show a slight increase in the density of microchaetae on the notum.
      (Escudero et al., 2003)
      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.
      (Bate et al., 1993)
      rl1/Df(2R)rl10a strongly enhances the wing phenotype of N55e11/+.
      (Diaz-Benjumea and Hafen, 1994)
      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.
      (de Celis and Garcia-Bellido, 1994)
      Cause a complex pleiotropic syndrome including perturbations of the chaetae pattern.
      (de Celis et al., 1991)
      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.
      (Hoch et al., 1994)
      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.
      (Couso and Martinez Arias, 1994)
      Thickened vein mutant.
      (Sturtevant and Bier, 1995)
      Instead of forming distinct invagination folds, the N mutant stomodeal nervous system anlage invaginates en masse.
      (Gonzalez-Gaitan and Jaeckle, 1995)
      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.
      (Rulifson and Blair, 1995)
      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}.
      (Guo et al., 1996)
      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.
      (de Celis et al., 1996)
      Heterozygotes show thickening of the wing veins, occasional terminal nicking of the wing, and 1-4 ectopic bristles on the wing surface.
      (Abu-Issa and Cavicchi, 1996)
      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.
      (Frise et al., 1996)
      Wing nicking phenotype.
      (Long et al., 1996)
      Heterozygotes have a triangular expansion of the veins at the wing margin, and approximately 25% of flies have notched wings.
      (Murata et al., 1996)
      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.
      (Giebel et al., 1997)
      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.
      (Seugnet et al., 1997)
      Embryos exhibit supernumerary md neurons that derive from ASC precursors.
      (Vervoort et al., 1997)
      Hemizygous lethal. Heterozygotes have a neurogenic phenotype and have a marked increase in the number of bristles on the notum.
      (Brennan et al., 1997)
      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.
      (Stuttem and Campos-Ortega, 1997)
      Homozygous embryos have an increased number of cardiac precursor cells.
      (Jagla et al., 1997)
      Heterozygotes show scalloping of the wing margin and thickening of the wing veins.
      (Sotillos et al., 1997)
      N55e11/Df(1)N-8 transheterozygotes exhibit ectopic bristles on the notum.
      (Rottgen et al., 1998)
      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).
      (Zeng et al., 1998)
      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.
      (Martinez Arias, 1998)
      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.
      (Boube et al., 1998)
      Wing veins are thickened.
      (Roch et al., 1998)
      The segmental border muscle progenitors do not segregate at all or do not divide properly.
      (Jagla et al., 1998)
      Multiple Malpighian tubule tip cells develop in homozygous embryos.
      (Hoch and Jackle, 1998)
      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).
      (Rusconi and Corbin, 1998)
      Nl1N-ts1/N55e11 wing discs show a reduction in the size of the pouch. Heterozygotes show mild notching of the distal wing margin.
      (Nagaraj et al., 1999)
      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.
      (Llimargas, 1999)
      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.
      (Bishop et al., 1999)
      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.
      (Rauskolb and Irvine, 1999)
      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.
      (zur Lage and Jarman, 1999)
      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.
      (Micchelli and Blair, 1999)
      Homozygous mutant clones in the wing disc fail to respect the dorsal ventral boundary.
      (Rauskolb et al., 1999)
      Mutant embryos show severe hyperplasia of the central and peripheral nervous systems.
      (Le Gall and Giniger, 2004)
      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.
      (Rusconi and Corbin, 1999)
      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.
      (de Celis and Bray, 2000)
      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.
      (Udolph et al., 2001)
      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.
      (Lopez-Schier and St. Johnston, 2001)
      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.
      (Grammont and Irvine, 2001)
      In mutant clones in the follicle cells the organization of the spectrin cytoskeleton is normal.
      (Lopez-Schier and St. Johnston, 2002)
      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.
      (Deng et al., 2001)
      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).
      (Sudarsan et al., 2002)
      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.
      (Umesono et al., 2002)
      Mutant embryos completely lack hindgut boundary cell rows and rings.
      (Iwaki and Lengyel, 2002)
      Heterozygotes lack vein and sensory bristle tissue at the most distal tip of the wing.
      (Glise et al., 2002)
      N55e11/Nl1N-ts1 flies form ectopic abdominal ventral multidendritic neurons and pI external sensory organ precursor cells, even when raised at 19oC.
      (Orgogozo et al., 2002)
      The number of crystal cell precursors seen in mutant lymph glands is significantly reduced.
      (Lebestky et al., 2003)
      Pupal lethal when heterozygous with the MBT chromosome.
      (Riede, 2001)
      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.
      (Crozatier et al., 2003)
      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.
      (Fuss et al., 2004)
      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.
      (Stute et al., 2004)
      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.
      (Torres et al., 2003)
      N55e11/+ mutant flies have notches in the wing margin. These notches are more pronounced when flies carry the Df(3L)Ar14-8 deficiency.
      (Weber et al., 2003)
      Heterozygotes have a wild-type bristle pattern.
      (Tian et al., 2004)
      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.
      (Adam and Montell, 2004)
      N55e11 germline clones and N55e11 zygotic mutants exhibit crystal cells.
      (Bataille et al., 2005)
      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.
      (Ohlstein and Spradling, 2006)
      Somatic clones of N[55e11] in mid-third instar larvae have normal numbers and distribution of postembryonic neuroblasts.
      (Almeida and Bray, 2005)
      Female flies heterozygous for N[55e11] show moderate scalloping of the wing, thickened wing vein L3, and duplicated anterior and posterior scutellar macrochaetae.
      (Kamimura et al., 2004)
      Homozygous intestinal stem cell (ISC) clones in the adult midgut form tumours.
      (Ohlstein and Spradling, 2007)
      The number of fusion competent myoblasts is decreased in stage 11 N[55e11] embryos.
      (Beckett and Baylies, 2006)
      N[55e11] mutant germline stem cells are maintained in the niche similarly to wild-type control clones.
      (Ward et al., 2006)
      hide Interactions
      hide Phenotypic Class
      hideEnhanced by
      Statement
      Reference
      N55e11 has visible | dominant phenotype, enhanceable by kuz1405Rev4/kuz1405Rev11
      (Sotillos et al., 1997)
      Df(1)N-8/N55e11 has visible phenotype, enhanceable by eIF-4a162-3
      (Rottgen et al., 1998)
      Df(1)N-8/N55e11 has visible phenotype, enhanceable by ptcE227-2
      (Rottgen et al., 1998)
      Df(1)N-8/N55e11 has visible phenotype, enhanceable by ptcE291-6
      (Rottgen et al., 1998)
      Df(1)N-8/N55e11 has visible phenotype, enhanceable by ptcE470-3
      (Rottgen et al., 1998)
      Df(1)N-8/N55e11 has visible phenotype, enhanceable by ptcX234-1
      (Rottgen et al., 1998)
      Df(1)N-8/N55e11 has visible phenotype, enhanceable by ptcX253-4
      (Rottgen et al., 1998)
      Df(1)N-8/N55e11 has visible phenotype, enhanceable by l(2)44DEaE305-3
      (Rottgen et al., 1998)
      Df(1)N-8/N55e11 has visible phenotype, enhanceable by Hr46k09242
      (Rottgen et al., 1998)
      N55e11 has visible | dominant phenotype, enhanceable by RpL15[+]/RpL1572
      (Schulze et al., 2005)
      N55e11, RpL15[+]/RpL1572 has visible | dominant phenotype, enhanceable by Su(var)2051
      (Schulze et al., 2005)
      N55e11 has visible phenotype, enhanceable by Scer\GAL4dpp.blk1/Hs3st-BdsRNA.IR.Scer\UAS
      (Kamimura et al., 2004)
      hideSuppressed by
      Statement
      Reference
      N55e11 has visible phenotype, suppressible by HC21
      (Price et al., 1997)
      N55e11 has visible phenotype, suppressible by HC24
      (Price et al., 1997)
      N55e11 has visible phenotype, suppressible by HC57
      (Price et al., 1997)
      N55e11 has visible phenotype, suppressible by HC73
      (Price et al., 1997)
      N55e11 has visible phenotype, suppressible by vnC221
      (Price et al., 1997)
      N55e11 has visible phenotype, suppressible by E(Egfr)B56B56
      (Price et al., 1997)
      N55e11 has visible phenotype, suppressible by E(Egfr)C12C12
      (Price et al., 1997)
      N55e11 has visible phenotype, suppressible by E(Egfr)C22C22
      (Price et al., 1997)
      N55e11 has visible | dominant phenotype, suppressible by Dsor1Su1
      (Nagaraj et al., 1999)
      N55e11 has visible | dominant phenotype, suppressible by wgS107
      (Brennan et al., 1997)
      N55e11 has visible | dominant phenotype, suppressible by DlM1/Dl[+]
      (de Celis and Bray, 2000)
      hideEnhancer of
      Statement
      Reference
      N55e11 is an enhancer of visible phenotype of CG17667EP3622, Scer\GAL4sca-537.4
      (Abdelilah-Seyfried et al., 2000)
      N55e11 is an enhancer of visible phenotype of EP595aEP595a, Scer\GAL4sca-537.4
      (Abdelilah-Seyfried et al., 2000)
      N55e11 is an enhancer of visible phenotype of GliEP2306, Scer\GAL4sca-537.4
      (Abdelilah-Seyfried et al., 2000)
      N55e11 is an enhancer of visible phenotype of EP595bEP595b, Scer\GAL4sca-537.4
      (Abdelilah-Seyfried et al., 2000)
      N55e11 is an enhancer of visible phenotype of Scer\GAL4sca-537.4, blEP954
      (Abdelilah-Seyfried et al., 2000)
      N55e11 is an enhancer of visible phenotype of Scer\GAL4sca-537.4, spenEP2583
      (Abdelilah-Seyfried et al., 2000)
      N55e11 is an enhancer of visible phenotype of Scer\GAL4sca-537.4, trblEP3519
      (Abdelilah-Seyfried et al., 2000)
      N[+]/N55e11 is an enhancer of visible | somatic clone phenotype of emc1
      (Baonza et al., 2000)
      argosΔ7, argos[+], N[+], N55e11 is an enhancer of tissue polarity defective phenotype of Cct116919
      (Weber et al., 2003)
      N[+]/N55e11 is an enhancer of visible | recessive phenotype of rumi44
      (Acar et al., 2008)
      hideNOT Enhancer of
      Statement
      Reference
      N[+]/N55e11 is a non-enhancer of visible phenotype of BEST:SD02913EP2437, Scer\GAL4sca-537.4
      (Abdelilah-Seyfried et al., 2000)
      N[+]/N55e11 is a non-enhancer of