A Database of Drosophila Genes & Genomes

FB2008_07, released August 8, 2008
 

Allele Dmel\Nl1N-ts1

General Information
SymbolDmel\Nl1N-ts1SpeciesD. melanogaster
NameFlyBase IDFBal0012887
Feature typealleleCreated / Updated2006-08-22/2006-08-22
Associated geneDmel\N
Allele classloss of function, hypomorph
Mutagenethyl methanesulfonate
hide Nature of the Allele
Allele class
loss of function
(Lehmann et al., 1983, Baker and Yu, 1997, Kenyon et al., 2003)
hypomorph
(Heitzler and Simpson, 1991, Heitzler et al., 1996, Kamimura et al., 2004)
Mutagen
ethyl methanesulfonate
(Shellenbarger and Mohler, 1975)
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
      Amino acid replacement: G1272D. G1272 falls in EGF repeat number 32.
      (Couso and Martinez Arias, 1994)
      Amino acid replacement: G1272D.
      (Baker and Zitron, 1995, Baker and Yu, 1997)
      Amino acid replacement: G1272D. Residue G1272 is within the 32nd EGF-like repeat.
      (Heitzler et al., 1996)
      Missense mutation in the extracellular domain.
      (Menne and Klambt, 1994, Schweisguth et al., 1996)
      Nucleotide substitution: G4556A. Amino acid replacement: G1272D. G1272D coordinates according to FBrf0042040. This change is within the 32nd EGF-like repeat.
      (Xu et al., 1992)
      Assay mode
      Cytology
      hide Phenotypic Data
      hide Phenotypic Class
      lethal (with N55e11)
      (Micchelli and Perrimon, 2006)
      lethal (with N264-47)
      (Micchelli and Perrimon, 2006)
      lethal | recessive | conditional - heat sensitive
      (Held, 1990, Shellenbarger and Mohler, 1975, Giniger, 1998, Held, 1990)
      lethal | conditional - heat sensitive
      (Rulifson and Blair, 1995, Heitzler and Simpson, 1991)
      lethal | neurogenic | recessive | conditional - heat sensitive
      (Couso and Martinez Arias, 1994)
      lethal | embryonic stage | neurogenic | recessive
      (Lehmann et al., 1983)
      visible
      (Schweisguth et al., 1996, Pi et al., 2001)
      visible (with NMcd8)
      (Ramain et al., 2001)
      visible (with NMcd5)
      (Ramain et al., 2001)
      visible (with NMcd1)
      (Ramain et al., 2001)
      visible | recessive | conditional - heat sensitive
      (Reddy and Rodrigues, 1999, Held, 1990, Held, 1990, Ligoxygakis et al., 1999, Tomlinson and Struhl, 1999, Bishop et al., 1999)
      visible | dominant
      (Kamimura et al., 2004)
      visible | temperature conditional
      (Kamimura et al., 2004)
      visible | conditional - heat sensitive
      (Periz and Fortini, 1999, Couso et al., 1995, Barolo et al., 2002)
      visible | conditional - heat sensitive (with Df(1)N-81k1)
      (Barolo et al., 2000)
      visible | neurogenic | somatic clone
      (Seugnet et al., 1997)
      female sterile | conditional - heat sensitive
      (Ruohola et al., 1991)
      memory defective
      (Presente et al., 2004)
      courtship defective
      (Presente et al., 2004)
      cell death increase | recessive | conditional - heat sensitive
      (Ye and Fortini, 1999)
      cell death decrease | conditional - heat sensitive
      (Cordero et al., 2004)
      cell shape defective | conditional - heat sensitive
      (Major and Irvine, 2005)
      neuroanatomy defective
      (Parrish et al., 2006, Wang et al., 2006, Wang et al., 2007)
      neuroanatomy defective | conditional - heat sensitive
      (Edenfeld et al., 2007)
      immune response defective
      (Duvic et al., 2002)
      tissue polarity defective
      (Cooper and Bray, 1999, Fanto and Mlodzik, 1999)
      tissue polarity defective | recessive | conditional - heat sensitive
      (Tomlinson and Struhl, 1999)
      hide Phenotype Manifest In
      abdominal ventral multidendritic neuron | ectopic (with N55e11)
      (Orgogozo et al., 2002)
      external sensory organ precursor cell | ectopic (with N55e11)
      (Orgogozo et al., 2002)
      mechanosensory sensory organ
      (Merdes et al., 2004, van de Bor and Giangrande, 2001)
      ventral thoracic disc
      (zur Lage and Jarman, 1999)
      A subperineurial glial cell
      (Udolph et al., 2001)
      B subperineurial glial cell of abdomen
      (Udolph et al., 2001)
      lateral ventral subperineurial glial cell
      (Udolph et al., 2001)
      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)
      ovary
      (Cummings and Cronmiller, 1994)
      eye | conditional - heat sensitive
      (Periz and Fortini, 1999, Shellenbarger and Mohler, 1975, Tomlinson and Struhl, 1999)
      lens | conditional - heat sensitive
      (Periz and Fortini, 1999)
      eye | somatic clone
      (Dietrich and Campos-Ortega, 1984)
      ommatidium | somatic clone
      (Dietrich and Campos-Ortega, 1984)
      pigment cell | somatic clone
      (Dietrich and Campos-Ortega, 1984)
      macrochaeta & thorax | anterior | dorsal | somatic clone
      (Dietrich and Campos-Ortega, 1984)
      eye photoreceptor cell | somatic clone
      (Dietrich and Campos-Ortega, 1984)
      macrochaeta | somatic clone
      (Dietrich and Campos-Ortega, 1984)
      interommatidial bristle | somatic clone
      (Dietrich and Campos-Ortega, 1984)
      macrochaeta & thorax
      (Schweisguth et al., 1996)
      adult midgut
      (Micchelli and Perrimon, 2006, Ohlstein and Spradling, 2006)
      ectoderm
      (Bodmer et al., 1993)
      crystal cell & larva | conditional ts
      (Duvic et al., 2002)
      border follicle cell | conditional - heat sensitive
      (Schober et al., 2005)
      egg chamber
      (Jackson and Blochlinger, 1997, Zhao et al., 2000)
      RP2sib neuron
      (Wai et al., 1999, Buescher et al., 1998)
      embryonic/larval somatic muscle
      (Fuerstenberg and Giniger, 1998)
      embryonic trachea
      (Llimargas, 1999)
      ommatidium
      (Cooper and Bray, 1999, Fanto and Mlodzik, 1999)
      photoreceptor cell R4
      (Cooper and Bray, 1999, Fanto and Mlodzik, 1999)
      dorsal mesothoracic disc | conditional - heat sensitive
      (Ye and Fortini, 1999, Ligoxygakis et al., 1999)
      embryonic/larval dorsal branch
      (Steneberg et al., 1999, Ikeya and Hayashi, 1999)
      microtubule & oocyte
      (Larkin et al., 1999)
      basal stalk
      (Larkin et al., 1999, Goode et al., 1996, Larkin et al., 1996)
      nurse follicle cell
      (Larkin et al., 1999)
      scutum & microchaeta & trichogen cell | conditional ts
      (Reddy and Rodrigues, 1999)
      scutum & microchaeta & tormogen cell | conditional ts
      (Reddy and Rodrigues, 1999)
      larval brain
      (Hassan et al., 2000)
      mesothoracic tarsal segment 1 | conditional - heat sensitive
      (Held, 1990)
      mesothoracic tarsal bristle | conditional - heat sensitive
      (Held, 1990, Held, 1990)
      cardiogenic mesoderm
      (Mandal et al., 2004)
      lymph gland primordium
      (Mandal et al., 2004)
      embryonic pericardial cell
      (Mandal et al., 2004)
      cardioblast
      (Mandal et al., 2004)
      lymph gland
      (Mandal et al., 2004)
      microchaeta | somatic clone
      (Seugnet et al., 1997)
      embryonic/larval dorsal branch & tracheal tip cell
      (Ikeya and Hayashi, 1999)
      embryonic/larval lateral trunk
      (Ikeya and Hayashi, 1999)
      embryonic/larval dorsal trunk
      (Ikeya and Hayashi, 1999)
      wing
      (Couso et al., 1995, Diaz-Benjumea and Cohen, 1995, Hartenstein and Posakony, 1990)
      microchaeta & scutum
      (Couso et al., 1995)
      primary pigment cell | conditional - heat sensitive
      (Cordero et al., 2004)
      eye disc | conditional - heat sensitive
      (Cordero et al., 2004)
      ommatidial cluster | conditional - heat sensitive
      (Cordero et al., 2004)
      perineural sheath cell
      (Guo et al., 1996)
      labellum & macrochaeta
      (Ray and Rodrigues, 1994)
      larval stomatogastric nervous system
      (Hartenstein et al., 1996)
      tarsal segment
      (de Celis Ibeas and Bray, 2003)
      embryonic/first instar larval cuticle
      (Martinez Arias, 1998)
      embryonic epidermis
      (Lehmann et al., 1983)
      leg | conditional - heat sensitive
      (Shellenbarger and Mohler, 1975, Bishop et al., 1999)
      head | conditional - heat sensitive
      (Shellenbarger and Mohler, 1975)
      ommatidium | conditional - heat sensitive
      (Shellenbarger and Mohler, 1975, Tomlinson and Struhl, 1999)
      microchaeta | supernumerary
      (Pi et al., 2001)
      embryonic neuron | supernumerary
      (Pi et al., 2001)
      dorsal mesothoracic disc
      (Micchelli and Blair, 1999, Nagaraj et al., 1999)
      chaeta | conditional - heat sensitive
      (Barolo et al., 2002)
      centripetally migrating follicle cell | conditional - heat sensitive
      (Dobens et al., 2005)
      chorion | conditional - heat sensitive
      (Dobens et al., 2005)
      dorsal appendage | conditional - heat sensitive
      (Dobens et al., 2005)
      nurse cell | conditional - heat sensitive
      (Dobens et al., 2005)
      nurse follicle cell | conditional - heat sensitive
      (Dobens et al., 2005)
      oocyte associated follicle cell | conditional - heat sensitive
      (Dobens et al., 2005)
      dorsal mesothoracic disc | dorsal/ventral compartment boundary | conditional - heat sensitive
      (Major and Irvine, 2005)
      dorsal mesothoracic disc & filamentous actin | conditional ts
      (Major and Irvine, 2005)
      mechanosensory sensory organ & wing vein L1 & glial cell | supernumerary
      (van de Bor and Giangrande, 2001)
      chemosensory sensory organ & wing vein L1 & glial cell | supernumerary
      (van de Bor and Giangrande, 2001)
      mechanosensory sensory organ & wing vein L3 & glial cell | supernumerary
      (van de Bor and Giangrande, 2001)
      chemosensory sensory organ & wing vein L3 & glial cell | supernumerary
      (van de Bor and Giangrande, 2001)
      external sensory organ precursor cell
      (van de Bor and Giangrande, 2001)
      external sensory organ precursor cell IIa
      (van de Bor and Giangrande, 2001)
      trichogen cell
      (van de Bor and Giangrande, 2001)
      tormogen cell
      (van de Bor and Giangrande, 2001)
      thecogen cell
      (van de Bor and Giangrande, 2001)
      eo neuron
      (van de Bor and Giangrande, 2001)
      eo neuron | supernumerary
      (van de Bor and Giangrande, 2001)
      longitudinal connective | conditional - heat sensitive
      (Giniger, 1998)
      eye-antennal disc
      (Kenyon et al., 2003, Cagan and Ready, 1989)
      sensillum trichodeum of antennal segment 3
      (Reddy et al., 1997)
      sensillum basiconicum of antennal segment 3
      (Reddy et al., 1997)
      sensillum coeloconica of antennal segment 3
      (Reddy et al., 1997)
      antenna
      (Reddy et al., 1997)
      sensory mother cell
      (Reddy et al., 1997)
      sacculus | ectopic
      (Reddy et al., 1997)
      sensory mother cell | ectopic
      (Reddy et al., 1997)
      photoreceptor cell R8
      (Baker and Yu, 1997, Baker and Yu, 1998, Baker et al., 1996, Baker and Zitron, 1995)
      dorsal medial muscle
      (Anant et al., 1998)
      lateral oblique dorsal muscle
      (Anant et al., 1998)
      tergosternal muscle
      (Anant et al., 1998)
      coxal tergal remotor muscle
      (Anant et al., 1998)
      oocyte
      (Xu et al., 1992)
      dorsal appendage
      (Xu et al., 1992, Zhao et al., 2000, Jordan et al., 2000)
      ovariole
      (Xu et al., 1992)
      dorsal pouch
      (Diaz-Benjumea and Cohen, 1995)
      microchaeta
      (Hartenstein and Posakony, 1990)
      macrochaeta
      (Hartenstein and Posakony, 1990)
      leg
      (Hartenstein and Posakony, 1990)
      adult head
      (Hartenstein and Posakony, 1990)
      tarsal segment 1 | conditional - heat sensitive
      (Held, 1990)
      follicle cell
      (Zhao et al., 2000, Gonzalez-Reyes and St. Johnston, 1998)
      wing | conditional - heat sensitive
      (Ligoxygakis et al., 1999)
      photoreceptor cell R3 | conditional - heat sensitive
      (Tomlinson and Struhl, 1999)
      photoreceptor cell R4 | conditional - heat sensitive
      (Tomlinson and Struhl, 1999)
      photoreceptor cell | ectopic
      (Tsuda et al., 2002)
      cone cell
      (Tsuda et al., 2002)
      macrochaeta | conditional - heat sensitive
      (Berdnik et al., 2002)
      oocyte nucleus
      (Gonzalez-Reyes and St. Johnston, 1998)
      cardioblast | supernumerary
      (Tian et al., 2004)
      egg | anterior | dorsal
      (Jordan et al., 2000)
      microchaeta & antennal segment 3 | conditional ts
      (Sen et al., 2003)
      glial cell & antennal segment 3 | ectopic | conditional ts
      (Sen et al., 2003)
      fascicle & antennal segment 3 | conditional ts
      (Sen et al., 2003)
      anterior fascicle | conditional - heat sensitive
      (Crowner et al., 2003, Edenfeld et al., 2007)
      embryonic nervous system
      (Buescher et al., 1998)
      pCC neuron
      (Buescher et al., 1998)
      ventral midline
      (Menne et al., 1997)
      neuromere
      (Menne et al., 1997)
      prothoracic tibial apical bristle | conditional - heat sensitive
      (Bishop et al., 1999)
      mesothoracic tibial apical bristle | conditional - heat sensitive
      (Bishop et al., 1999)
      eye
      (Cagan and Ready, 1989)
      primary pigment cell
      (Cagan and Ready, 1989)
      secondary pigment cell
      (Cagan and Ready, 1989)
      dorsal multidendritic neuron ddaD | supernumerary
      (Parrish et al., 2006)
      dorsal multidendritic neuron ddaE | supernumerary
      (Parrish et al., 2006)
      wing vein L3
      (Kamimura et al., 2004)
      anterior scutellar bristle
      (Kamimura et al., 2004)
      posterior scutellar bristle
      (Kamimura et al., 2004)
      embryonic/larval dorsal branch | conditional - heat sensitive
      (Ghabrial and Krasnow, 2006)
      peripheral glial cell | conditional - heat sensitive
      (Edenfeld et al., 2007)
      neuroblast & larval brain
      (Wang et al., 2006)
      neuroblast
      (Wang et al., 2007)
      adult thorax & microchaeta (with NMcd1)
      (Ramain et al., 2001)
      adult thorax & microchaeta (with NMcd5)
      (Ramain et al., 2001)
      adult thorax & microchaeta (with NMcd8)
      (Ramain et al., 2001)
      cardioblast | supernumerary (with Df(1)N-81k1)
      (Tian et al., 2004)
      tormogen cell | conditional - heat sensitive (with Df(1)N-81k1)
      (Barolo et al., 2000)
      trichogen cell | ectopic | conditional - heat sensitive (with Df(1)N-81k1)
      (Barolo et al., 2000)
      hide Detailed Description
      Statement
      Reference
      Temperature shifts of mature larvae result in most ommatidial cells becoming photoreceptors (Cagan and Ready, 1989). Nl1N-ts1/+ females are wild type at 18oC and 29oC, while Nl1N-ts1/Df(1)N-8 females are lethal at 29oC, but a few escapers are found at 18oC. Nl1N-ts1 homozygotes are viable at 18oC, but lethal at 29oC. If homo- and hemizygotes kept at 18oC until eclosion are transferred to 29oC and kept at this temperature for six days, they gradually become flightless and show gross histological changes in the flight muscles (Vikki and Portin, 1987). Heterozygotes show recessive visible defects at 18oC, but not at 29oC. Nl1N-ts1/Nl1N-2 and Nl1N-ts1/Nl1N-3 females survive until the late pupal stage at 29oC. When heat pulses are given to pupae prior to sensillum-precursor-cell-determination, extra sensilla are produced; when given after sensillum-precursor-cell determination, the precursor cells form neurons only, not accessory cells (Hartenstein and Posakony, 1990).
       
      Lethal in combination with Df(1)N-8 at both 18oC and 29oC. Homozygous lethal at 29oC (96% survive at 18oC). Wings are normal in heterozygotes. Homozygotes are morphologically normal at 18oC. 7% of Nl1N-2/Nl1N-ts1 flies survive at 29oC. Phenotypes seen include fused stubby legs and no head. 14% of Nl1N-3/Nl1N-ts1 flies survive at 29oC. Phenotypes seen include fused stubby legs, a small head and small, rough eyes. 5% of Nl1N-69e/Nl1N-ts1 flies survive at 29oC. Phenotypes seen include small, rough eyes and stubby legs. 2% of NAx-tsl/Nl1N-ts1 flies survive at 29oC. Phenotypes seen include stubby legs and an abruptex phenotype. Lethal in combination with N55e11, N264-39, N264-40, N60g11, N69d5, N69e2, NAx-59d, Nl1N-B or Nl1N-ts2 at 29oC. Nl1N-ts1 and NAx-tsl show negative complementation at 18oC; Nl1N-ts1/NAx-tsl flies do not survive as well as either homozygote.
      (Shellenbarger and Mohler, 1975)
      Weak embryonic neurogenic phenotype at 29oC.
      (Lehmann et al., 1983)
      Homozygous clones induced in the eye and thoracic imaginal discs show epidermal development indistinguishable from wild-type at 18oC. Homozygous clones in the eye have a severely disturbed ommatidial pattern, visible as a scar in the eye surface at 29oC. Ommatidia are larger than wild-type and interommatidial bristles are missing. Each ommatidium contains more retinula cells and fewer pigment cells than wild-type. Each ommatidium contains more receptor cells than normal, and may contain up to 13 receptor cells. Homozygous clones in the cuticle of the anterior dorsal thorax lack all bristles, while homozygous clones in other parts of the cuticle normally have additional bristles at the same positions as normal bristles at 29oC.
      (Dietrich and Campos-Ortega, 1984)
      Temperature shifts of third-instar larvae phenocopy the external defects of Nspl-1. Nearly all cells just posterior to the morphogenetic furrow in the eye differentiate into neurons which form large clusters in third instar Nl1N-ts1 larvae shifted to 32oC for 4 to 24 hours. Widespread neuralisation continues at the furrow as long as the flies are kept at the nonpermissive temperature. If the flies are shifted back to the permissive temperature, newly made clusters develop normally. The supernumerary neurons in animals shifted as larvae and then returned to the permissive temperature develop into clusters of rhabdomeres. A scar containing abnormal clusters is produced across the eye in adults shifted for at least 10 hours as larvae. Cell death occurs in the scar as the adult ages. Larval shifts produce mispositioned bristles and extra primary pigment cells in the eye, early pupal shifts 6-16hr after pupariation) produce extra bristles in the eye, and later pupal shifts (12-24hr after pupariation) produce bald eyes. Shifts starting 24hr after pupariation reduce the number of primary pigment cells and increase the number of secondary pigment cells.
      (Cagan and Ready, 1989)
      Heat pulses at the restrictive temperature (30oC) applied during the larval and early pupal stages have different effects on the pattern and structure of the adult epidermis, particularly the macro- and microchaetae, depending on the timing and length of the pulse. A heat pulse between 0 and 14hrs after puparium formation leads to an increase in microchaete precursors (which produce normal sensilla) at the expense of epidermal cells. Later heat pulses results in a hyperplasia of sensory neurons at the expense of accessory cells in the progeny of the sensillum precursors.
      (Hartenstein and Posakony, 1990)
      Homozygotes exposed to a 6 hour pulse of 29oC at ages ranging from a time equivalent to 0 to 10 hours after puparium formation at 25oC (AP25) have significantly more bristles on the basitarsus of the second leg than wild-type flies. With pulses initiated at 0 to 4 hours AP25, bristle density is greatest near the distal end of the segment. With pulses initiated at 5 to 10 hours AP25, bristle density is greatest near the middle of the segment. Bractless bristles are either missing completely (23% of total sites) or a socket is present without a shaft (9%) in flies exposed to a 6 hour pulse of 29oC at 0 to 5 hours AP25. Later pulses of 29oC (at 11 to 14 hours AP25) cause missing bracted bristles, and for these bristles, socketless shafts are four times more frequent than shaftless sockets. For flies exposed to a 6 hour pulse of 29oC at 15 or 16 hours AP25, the most frequent defect is a duplicated shaft lacking a socket. Pulses of 29oC started at 24 to 31 hours AP25 cause bractless bristles to acquire bracts.
      (Held, 1990)
      The basitarsi of the second legs are increased in width in flies derived from white prepupae aged for 10 hours and then exposed to the restrictive temperature of 31oC for 4 hours. The total number of bristles on the basitarsi of the second legs is increased and the number of bractless bristles is reduced. Bristles are no longer consistently aligned in rows. The bristle-less zone of sparse hairs between bristle rows 1 and 8 is narrower than normal.
      (Held, 1990)
      Mutant clones caused the differentiation of an excess of bristles at 29oC so more cells adopted a neural fate at the expense of epidermal cells. At 18oC fewer bristles are present that are widely spaced indicating more cells adopted the epidermal fate. Mutant cells autonomously adopt a neural fate in spite of the presence of neighbouring wild type cells. On the scutum N- clones fail to produce epidermis.
      (Heitzler and Simpson, 1991)
      Egg laying of Nl1N-ts1 homozygous females at the restrictive temperature (32oC) is greatly reduced. Germarium and vitellarium have morphological abnormalities. bcd mRNA is localized at the posterior end and there is no posterior localization of osk at the posterior at the restrictive temperature. Hyperplasia is seen in the specialized polar cells at the posterior end of an egg chamber in the vitellarium.
      (Ruohola et al., 1991)
      Homozygous females kept at non-permissive temperatures for three days do not produce any fertile eggs. After this time, almost all ovarioles appear abnormal, nurse cell-oocyte complexes appear fused into large irregular shapes, later stage oocytes appear abnormal, and the dorsal appendages are malformed. This sterility is reversible on return to the permissive temperature. The fertility of males is dramatically reduced after exposure to non-permissive temperatures.
      (Xu et al., 1992)
      In double mutant clones with Dl9P, both wild type and mutant bristles are formed along the mosaic borders, and occasionally a mutant and a wild type bristle are found adjacent to each other (which never happens in either single mutant).
      (Heitzler and Simpson, 1993)
      Epistatic to sgg32.
      (Ruel et al., 1993)
      At 30-32oC mutants exhibit 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. Replication is normal at 18oC.
      (Bodmer et al., 1993)
      Temperature shift experiments using Nl1N-ts1/Df(1)N-81k1 embryos reveals the visual system is sensitive to loss of N function between 6 and 10 hours after fertilisation (stages 11-13). Earlier heat pulses lead to a strong hyperplasia of the brains and ventral nerve cord, but no effect on the visual system. Temperature shifts about 6-8 hours cause overproduction of cells in Bolwig's organ and only mild effects in the optic lobes. Heat pulses between 7-9 and 8-10 hours do not cause a significant change in cell number in Bolwig's organ or optic lobe.
      (Green et al., 1993)
      90% of embryos exposed to the restrictive temperature between 2hrs and 3hrs after egg laying have normal epidermis but lack most of the midline cells and have fused longitudinal connectives, resembling the sim CNS mutant phenotype. Embryos exposed to the restrictive temperature after 3hrs after egg laying have midline cells form separate anterior and posterior commissures, though the longitudinal connectives are still not formed properly.
      (Menne and Klambt, 1994)
      Temperature-sensitive allele. Aberrant bristles are produced on the labellum if pupae are exposed to pulses of the restrictive temperature.
      (Ray and Rodrigues, 1994)
      Viable and fertile at 17oC. Embryonic lethal with neurogenic phenotype at 29oC. 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. When homozygous embryos are shifted from 17oC to 29oC during stage 10 they develop regions of ventral cuticle with extra denticles in the posterior region of many segments, similar to that seen for a decrease in wg activity during embryogenesis.
      (Couso and Martinez Arias, 1994)
      Nl1N-ts1/Nfa-g62 females show a sharply temperature-dependent facet-eye phenotype: eyes are wild type up to 23oC, but are facet-like at higher temperatures. Flies are fully viable and fertile at all temperatures tested.
      (Fortini and Artavanis-Tsakonas, 1994)
      Clusters of R8 cells develop in mutant flies raised at the restrictive temperature. The clusters are not randomly arranged, but are based on the original R8 array. The number of R8 cells is increased in scaBP2/scaUM2 Nl1N-ts1 or scaUM2/scaUM2 Nl1N-ts1 double mutants compared to Nl1N-ts1 single mutants, and no regular array of R8 cells can be seen. Extra R8 cells are produced in Nl1N-ts1 DlRF/Dl6B double mutants, although the number of extra R8 cells produced is somewhat reduced compared to Nl1N-ts1 single mutants.
      (Baker and Zitron, 1995)
      Flies raised at 17oC until the beginning of the second larval instar that are then transferred to 29oC exhibit wings that are reduced to stumps and rows of extra microchaetae in the notum.
      (Couso et al., 1995)
      Wing and wing pouch are reduced.
      (Diaz-Benjumea and Cohen, 1995)
      Temperature shifts reveal that neurogenic gene function is continuously required throughout SNS morphogenesis.
      (Hartenstein et al., 1996)
      Bristle multiplication phenotype on the thorax.
      (Schweisguth et al., 1996)
      Shifting embryos to 25oC at 4-5 hours of embryogenesis results in significant overproduction of neurons, sheath cells are transformed to neurons. Shift at 5-7 hours causes cell fate transformation within both es and cho lineages.
      (Guo et al., 1996)
      After shifting to the restrictive temperature for 7 hours a region of extensive neural hypertrophy is left behind as the morphogenetic furrow advances.
      (Baker et al., 1996)
      No stalks are formed in ovarioles allowed to develop at the restrictive temperature (32oC). Phenotype can be suppressed by constitutively active N, P{UAS-Dl::N.ΔECN} P{GAL4-Hsp70.PB}.
      (Larkin et al., 1996)
      Misappropriate development of stalk cells, stalk cells are not established no egg chambers fail to separate.
      (Goode et al., 1996)
      Antennal discs from pupae reared at 32oC for 0 to 6 hours after puparium formation (APF) contain increased numbers of sensory precursors, including ectopic olfactory sensilla founder cells. Adults derived from these pupae do not have any ectopic olfactory sense organs. The antenna is somewhat reduced in size in these flies, and there is a reduction in the number of sensilla basiconica and trichodea, and a slight increase in the number of sensilla coelonica. Pulses of high temperature between 7 and 17 hours APF result in a decrease in the number of antennal sensilla basiconica, trichodea and coelonica. Pulses of high temperature between 17 and 15 hours APF result in a decrease in the number of antennal sensilla basiconica and trichodea. A shift to non-permissive temperatures for 6 hours between 7 and 25 hours APF results in ectopic formation of the sacculus. A shift to the non-permissive temperature between 16 and 25 hours gives rise to several bifurcated sensilla on the third antennal segment.
      (Reddy et al., 1997)
      Behaves as a loss of function at the restrictive temperature (31.5oC). A short pulse at the restrictive temperature results in a zone of neural hypertrophy, corresponding to cells undergoing determination in the morphogenetic furrow at the time of the shift. The neurogenic phenotype is associated with an increased number of R8 photoreceptors. A less severe phenotype results from continued exposure. Proneural development is also affected in more anterior cells.
      (Baker and Yu, 1997)
      84% of the egg chambers of homozygous females maintained at the restrictive temperature for 64 hours are 'compound egg chambers'.
      (Jackson and Blochlinger, 1997)
      Ablation of the CNS midline anlage at stage 5. Heat shock reduces the average number of cells per neuromere from about 490 cells (wild type level) to 403-412 cells: mutants lack about 15% of the normal complement of lateral ventral cord cells.
      (Menne et al., 1997)
      Homozygous clones exhibit a strong neurogenic phenotype, all bristles at the border of the clone are mutant.
      (Seugnet et al., 1997)
      Homozygous viable at 18oC. Axonal defects occur in >90% of Nl1N-ts1 embryos shifted to the restrictive temperature after neuroblast segregation. This phenotype is rescued to wild type or nearly wild type in >80% of Nl1N-ts1; Scer\GAL4elav.PLu; NScer\UAS.cBa embryos. Scer\GAL4elav.PLu; NScer\UAS.cBa cannot rescue N-dependent defects in cell identity.
      (Giniger, 1998)
      Pupae shifted to the non-permissive temperature between 0-18 hours after puparium formation (APF) do not show splitting of the three larval templates for the dorsal longitudinal muscles (DLMs) which is seen in wild-type pupae. The DLMs differentiate as three "un-split" fibres in Nl1N-ts1 animals shifted to the non-permissive temperature between 0-18 hours APF. The dorsoventral muscles are sometimes mis-aligned and attach to each other or the DLMs. The direct flight muscles are normal.
      (Anant 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)
      aCC/pCC and RP2/RP2sib cell fates are correctly resolved in homozygous embryos raised at the permissive temperature (18oC). Embryos shifted to the non-permissive temperature (29oC) 2-4 hours after egg laying show sibling cell fate transformations and general hypertrophy of the nervous system. pCC to aCC and RP2sib to RP2 transformations are seen. The unequal size of the GMC4-2a daughter cells remains unaffected.
      (Buescher et al., 1998)
      The oocyte nucleus often remains at the posterior end in homozygous egg chambers raised at the restrictive temperature. The anteriormost follicle cells do not round up and fail to migrate between the nurse cells towards the oocyte.
      (Gonzalez-Reyes and St. Johnston, 1998)
      Shifts to the restrictive temperature early during embryogenesis result in hyperplasia of muscle progenitor cells. A shift to the restrictive temperature after the muscle progenitor cells are specified results in severe disruption of the mature muscle pattern.
      (Fuerstenberg and Giniger, 1998)
      Eye discs maintained at the restrictive temperature contain extra R8 photoreceptor cells.
      (Baker and Yu, 1998)
      Nl1N-ts1 flies which have been incubated at 30oC for 6 hours during the late third larval instar stage show some neural hypertrophy in the ommatidia. In addition, symmetrical ommatidia with the elongated shape expected for ommatidia containing two R3 photoreceptor cells are seen.
      (Cooper and Bray, 1999)
      Nl1N-ts1 flies raised at 25oC have ommatidia with the normal number of photoreceptor cells, but the ommatidia are sometimes symmetrical, having an R3/R3-like phenotype.
      (Fanto and Mlodzik, 1999)
      Nl1N-ts1/N55e11 wing discs show a reduction in the size of the pouch.
      (Nagaraj et al., 1999)
      Morphological abnormalities are seen in some nurse cell associated follicle cells in Nl1N-ts1 egg chambers incubated at the restrictive temperature. Abnormal microtubule organisation is seen in Nl1N-ts1 oocytes at the restrictive temperature. No stalk cells are detected in Nl1N-ts1 ovarioles.
      (Larkin et al., 1999)
      Nl1N-ts1 animals reared at 22oC for 18.5 hours and then pulsed at 30oC for 6 hours develop into adults that lack the external structures of several notal microchaetae.
      (Reddy and Rodrigues, 1999)
      Hemizygous flies shifted to the non-permissive temperature at the early third larval instar stage (72-84 hours after egg laying) have long paddle-shaped wings with extensive anterior and posterior scalloping. Hemizygous flies shifted to the non-permissive temperature at the mid third larval instar stage (96-108 hours after egg laying) show wing nicking around the margin, and show less extensive loss of wing tissue than flies shifted to the non-permissive temperature at the early third larval instar stage. The wing pouch is smaller than normal in wing discs shifted to the non-permissive temperature 72 hours after egg laying.
      (Ligoxygakis et al., 1999)
      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.
      (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)
      If mutants are shifted to the restrictive temperature just before division of GMC1 into RP2/Sib, both progeny assume an RP2 identity in about 60% of hemisegments. In about 70% of these cases the two cells occupy different planes on the dorsoventral and anteroposterior axis. The size asymmetry seen in wildtype is also less faithful.
      (Wai et al., 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)
      Embryos shifted to the restrictive temperature at stage 11 show tracheal defects. A misrouting defect is seen in the dorsal branch (DB). DBs are often curved in the anteroposterior direction and make contact with the tip of the DB from the same side of the embryo (in wild type the DB normally elongates to the dorsal midline where it meets its counterpart from the other side of the metamere). The misrouted DBs accumulate a luminal component but do not appear to fuse properly. Cell migration defects are also seen in the DB; the number of cells at the tip are increased with a corresponding decrease in the number of stalk cells, the latter having become unusually elongated (the total number of cell nuclei is not different from control embryos). The fine luminal extensions characteristic of terminal branches are often absent in the DBs of these embryos. Each fusion point in the dorsal branch, dorsal trunk and lateral trunk contains 2-4 extra esg-positive cells. No extra esg-positive cells are seen in the visceral branch or ganglionic branch.
      (Ikeya and Hayashi, 1999)
      In embryos subjected to the restrictive temperature for 1 hour, at stage 11-12, extra fusion cells develop from the group of cells that normally remain at the stalk of the dorsal branch.
      (Steneberg et al., 1999)
      Increased levels of apoptosis correlated with progressive loss of N+ activity are seen in wing discs of Nl1N-ts1 larvae shifted to the restrictive temperature.
      (Ye and Fortini, 1999)
      Homozygous Nl1N-ts1 wing discs have a wing pouch which is reduced in size. If grown at the restrictive temperature for the last 48 or 72 hours of larval development, the dorsal/ventral boundary in the wing disc is disrupted.
      (Micchelli and Blair, 1999)
      Nl1N-ts1/Nfa-g62 flies show a temperature sensitive roughening of the eye.
      (Periz and Fortini, 1999)
      Third instar larvae maintained at the restrictive temperature (31oC) for 8 hours and then maintained at the permissive temperature develop into flies that have a large dorso-ventral scar in the eye. Immediately behind the scar, ommatidia of inappropriate chiral types are found, with a preponderance of ommatidia showing the symmetrical form. Symmetrical ommatidia of both apparent R3/R3 and R4/R4 types are seen.
      (Tomlinson and Struhl, 1999)
      Reducing N+ activity during larval development (using Nl1N-ts1) has no effect on the number, morphology or position of the dorsal cluster of ato-expressing neurons in the brain or on the formation of the commissure. However, defects are seen in axon branching out of the commissure into the optic lobe; excessive branching and defasciculation of the axon bundles entering the optic lobe are seen.
      (Hassan et al., 2000)
      80% of eggs laid by Nl1N-ts1 females after 14 hours at the restrictive temperature have defects in the dorsal anterior region. The strongest phenotype is a complete loss of dorsal appendages.
      (Jordan et al., 2000)
      Nl1N-ts1 females have defects in oogenesis including fused compound egg chambers, abnormal organisation (overproliferation) of posterior and anterior-dorsal follicle cells and abnormal chorionic appendages.
      (Zhao et al., 2000)
      Nl1N-ts1/Df(1)N-81k1 flies shifted to the restrictive temperature after 36 hours of pupal development at 18oC show a transformation of many presumptive tormogen (socket) cells to the trichogen (shaft) fate, resulting in double-shaft bristles.
      (Barolo et al., 2000)
      Nl1N-ts1 flies show a wild-type morphology, including a normal array of neurosensory bristles.
      (Ben-Yaacov et al., 2001)
      When embryos are shifted to the restrictive temperature after 6 hours of development the A-, B- and LV-SPGs are absent, though there is not a global lack of all CNS glial cells. When Nl1N-ts1 cells are transplanted into an otherwise wild type background, then moved to the restrictive temperature, pCCs are transformed into aCCs, extra neurons are produced at the expense of the subperineurial glial cells. The loss of subperineurial glial cells is not complete, as it was for N55e11.
      (Udolph et al., 2001)
      Heat shock between 1 and 13hrs after puparium formation results in a dramatic increase in the number of glial cells compared to wild type wings. The number of sensory organs is normal. Heat shock between 1 and 10hrs after puparium formation results in chemosensory organs having extra glial cells due to a transformation within the sensory organ lineage. Heat shock between 1 and 13hrs after puparium formation results most often, for the late, gliogenic mechanosensory sensory organs, in sensory organs of six repo-expressing glial cells. Occasionally the sense organs may have 5 or 6 cells, of which two to five are glial cells. No sense organs with four glial cells have been detected. Comparison of short heat shocks indicated that N is required throughout the development of gliogenic sensory organs. For heat shocks between 12hrs before puparium formation and white pupa, or between 18hrs and 6hrs before puparium formation, 40-60% of the non-gliogenic sensory organ lineages showed supernumerary neurons. The strongest phenotype shows a sensory organ with 6 cells, all neurons.
      (van de Bor and Giangrande, 2001)
      Nl1N-ts1 flies in which N activity has been eliminated during 6-12 hours after puparium formation have a significantly increased number of microchaetae. Mutant embryos raised at the restrictive temperature show an overproduction of neurons.
      (Pi et al., 2001)
      NMcd1/Nl1N-ts1 flies have 53.83 +/- 1.78 thoracic microchaetae per heminotum (compared to the wild-type number of 130.35 +/- 1.54). NMcd5/Nl1N-ts1 flies have 36.75 +/- 1.88 thoracic microchaetae per heminotum. NMcd8/Nl1N-ts1 flies have 91.83 +/- 1.28 thoracic microchaetae per heminotum.
      (Ramain et al., 2001)
      Nl1N-ts1/Y flies shifted to the non-permissive temperature after sensory organ precursor formation shoe a variety of bristle defects, including a "double shaft" phenotype and "balding".
      (Barolo et al., 2002)
      In mutants at the non-permissive temperature, overspecification of R cells is seen, as well loss of cone cell specification.
      (Tsuda 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)
      When maintained at 18oC (the permissive temperature) Nl1N-ts1 mutant late third instar (wandering) larvae have wild-type numbers of circulating plasmatocytes and crystal cells. However, when Nl1N-ts1 mutant larvae are shifted to 29oC (the restrictive temperature) at second instar: the number of crystal cells seen in the resulting late third instar larvae is significantly reduced compared to those in wild-type controls, as are the number of Bc expressing cells in larval lymph glands. Plasmatocyte numbers are not affected. The induction of lamellocytes 48 hours after parisitization of second instar larvae by the wasp L.boulardi is significantly reduced in Nl1N-ts1 raised at 29oC compared to wild-type, or to Nl1N-ts1 larvae raised at 18oC assayed 72-96 hours after parasitization.
      (Duvic et al., 2002)
      All macrochaetae are absent from the heads of Nl1N-ts1 flies raised at 29oC.
      (Berdnik et al., 2002)
      Mutant animals that have been subjected to the restrictive temperature, exhibit a ISNb axon bypass phenotype. These axons reach their targets via an aberrant trajectory, in which ISNb axons remain associated with the ISN. The expressivity of the phenotype can be up to about 3/4, depending on when the embryos are raised to the restrictive temperature. The formation of neuromuscular synapses to ventral longitudinal muscles occur as efficiently in mutant animals than in controls. Other kinds of ISNb misrouting phenotypes are seen at a low frequency (~4% of hemisegments). However gross stalling of ISNb axons is not seen, nor are defects in muscle development.
      (Crowner et al., 2003)
      When Nl1N-ts1 animals are pulsed at 32o