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Allele Dmel\Nl1N-ts1
| General Information | |||
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| Symbol | Dmel\Nl1N-ts1 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0012887 | |
| Feature type | allele | Associated gene | Dmel\N |
| Also Known As | Nts1, Nts, Nts-1, notchts, l(1)Nts1, Notchts1, l(1)Nts | ||
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| Allele class | heat sensitive hypomorphic allele - genetic evidence | ||
| Mutagen | ethyl methanesulfonate | ||
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| Description |
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| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
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Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mutations Mapped to the Genome | |||
Type Location Additional Notes References point mutation comment=Position of mutation on reference sequence inferred by FlyBase curator based on author statement. evidence=experimental na_change=G3060476A pr_change=G1272D|N-PA reported_na_change=G4556A reported_pr_change=G1272D | |||
| Associated Sequence Data | |||
| DDBJ
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
| UniProtKB/Swiss-Prot | |||
| UniProtKB/TrEMBL | |||
| Progenitor genotype | |||
| Nature of the lesion | Statement Reference Amino acid replacement: G1272D. Residue G1272 is within the 32nd EGF-like repeat. Amino acid replacement: G1272D. Amino acid replacement: G1272D. G1272 falls in EGF repeat number 32. Missense mutation in the extracellular domain. Nucleotide substitution: G4556A. Amino acid replacement: G1272D. G1272D coordinates according to FBrf0042040. This change is within the 32nd EGF-like repeat. | ||
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Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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adult thorax & microchaeta (with NMcd1) adult thorax & microchaeta (with NMcd5) adult thorax & microchaeta (with NMcd8) chemosensory sensory organ & wing vein L1 & glial cell | supernumerary chemosensory sensory organ & wing vein L3 & glial cell | supernumerary dorsal mesothoracic disc & filamentous actin | conditional ts embryonic/larval dorsal branch & tracheal tip cell fascicle & antennal segment 3 | conditional ts glial cell & antennal segment 3 | ectopic | conditional ts labellum & macrochaeta macrochaeta & thorax macrochaeta & thorax | anterior | dorsal | somatic clone mechanosensory sensory organ & wing vein L1 & glial cell | supernumerary mechanosensory sensory organ & wing vein L3 & glial cell | supernumerary microchaeta & antennal segment 3 | conditional ts microchaeta & scutum microtubule & oocyte neuroblast & larval brain scutum & microchaeta & tormogen cell | conditional ts scutum & microchaeta & trichogen cell | conditional ts | |||
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Detailed Description
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Statement Reference N[l1N-ts1] animals raised at the restrictive temperature from 12 hours after puparium formation onwards and expressing N[Scer\UAS.cUa] under the control of Scer\GAL4[neur-GAL4-A101] (to restore N activity selectively in the sensory organs) show normal development of the majority of mechanosensory organs of the leg, and each of these correctly induces a single proximal bract. Late third instar N[l1N-ts1] mutant wing discs exhibit increased boundary cell proliferation, compromising the dorsal-ventral affinity boundary. Mutant females raised at 22[o]C show an increase in microchaeta density on the notum, with approximately 6-7 disorganised rows of microchaetae from the midline to the dorsocentral macrochaetae.
At 25[o]C, N[l1N-ts1] animals show pupal lethality. Mature longitudinal axon tracts of homozygous N[l1N-ts1] mutant embryos shifted to the restrictive temperature midway through embryogenesis fail to form. Examining embryos at early stage 13 reveal that the phenotype is apparent at the earliest stages of the pioneering of these tracts. In temperature shifted N[l1N-ts1] embryos, the dMP2 and vMP2 axons grow in the appropriate direction, but stall, failing to make contact even by late stage 13. Expressivity of this phenotype depends on the timing of the temperature shift.
Expression of N[dsRNA.Scer\UAS.cUa] under the control of Scer\GAL4[repo-M1B] enhances the N[l1N-ts1] early axon phenotype.
N[l1N-ts1] embryos have the normal number of interface glia. The position and morphology of those glia appear largely normal.
In wild-type embryos, the longitudinal axon growth cones do not directly contact the interface glia, but rather a thin meshwork of neuronal tissue intervenes between. In N[l1N-ts1] mutants, while this neuronal meshwork forms within each segmental ganglion, it does not spread laterally between ganglia to make an unbroken band stretching from segment to segment. Instead, there are gaps in the mesh between segments, and pioneer axons often (but not always) stall or misroute when they encounter those gaps. Interface glia are still present in segments with stalled axons even though the neuronal meshwork is absent.
There are fewer and shorter filopodia on dMP2 growth cones of N[l1N-ts1] mutants as compared with wild-types. The gonads of mutant male larvae show a reduction in hub cell number when grown at the non-permissive temperature compared to controls raised at the permissive temperature. A reduction in the number of neuroblasts is seen when N[l1N-ts1] is shifted to the restrictive temperature from the first instar larval stage onwards. N[l1N-ts1] mutant axons often grow past the 'choice point' at which they should exit the main ISN and enter the ventrolateral muscle domain. This results in an abnormal 'bypass' innervation pattern, with few or no axon projections in to the ventrolateral muscle (in 36% of total defective hemi-segments) under appropriate temperature shifting conditions. Guidance errors also occur in segmental nerve a (SNa) in N[l1N-ts1] mutants. Homozygous animals raised at 25[o]C during embryogenesis and then shifted to 31[o]C show defects optic lobe development. The neuroepithelial cells in the outer proliferation center appear normal with regard to epithelial cell morphology and apical marker expression at the second instar stage, but the neuroepithelium does not subsequently expand and has largely disappeared by the mid-third larval instar. An increased number of medulla neuroblasts is seen in the mutant larvae compared to wild type during early to mid-third larval instar. Medulla neurogenesis occurs prematurely in the mutant optic lobes and by late-third instar there are very few medulla neuroblasts in the mutant compared to wild type. The lamina is absent and the medulla is smaller than normal (100% penetrance) in the mutant third larval instar optic lobe. The central brain and ventral nerve cord appear normal in these animals. The eye imaginal discs are very small. N[l1N-ts1] mutant animals shifted to the restrictive temperature for 3h exhibit abnormal initiation of R7 specification, however, maintenance of the R7 fate in cells where it has already initiated appears to be unaffected. N[l1N-ts1] mutant flies grown at 18[o]C and then shifted to 31[o]C (once 40% through pupal development) for 6 hours display normal retinal development. Expression of N[l1N-ts1] during second instar larval stage (controlled by shifting N[l1N-ts1] animals from 17[o]C to 29[o]C at the appropriate time) results in a strong reduction of eye disc size. Nl1N-ts1 mutant embryos that are shifted to the restrictive temperature at stage 12 show irregular positioning of the glial cells with a failure of the dorsal intersegmental peripheral glial cells to migrate ventrally. Concomitantly, there is a defasciculation of the intersegmental nerve, indicating glial differentiation defects. When Nl1N-ts1 embryos are shifted to the restrictive temperature at stage 11, they show an increase in the number of glial cells, which all show abnormal migration behavior. Nl1N-ts1 animals subjected to 29oC temperature show a partial loss of neuroblasts in the central brain. Flies hemizygous for N[l1N-ts1] raised at permissive temperatures show normal postorbital bristle morphology. When N[l1N-ts1] flies are shifted to the restrictive temperature during external sensory organ development hair and socket cells are transformed into inner cells and a loss of bristles is observed. Nl1N-ts1 embryos shifted to the non-permissive temperature for 6 hours during tracheal branch budding show migration of additional cells to the dorsal branch tip. Loss of wg expression in the DV boundary of wing imaginal disc of N[l1N-ts1] mutants grown at restrictive temperature abolishes apical cell shape, with the cells being apically constricted. Homozygous adults are produced at the permissive temperature, and the midguts are similar to wild type. Homozygotes shifted to the non-permissive temperature have a mild increase in the number of small cells in the adult midgut epithelium. Nl1N-ts1/Nnd-1 adults are produced at the permissive temperature. Nl1N-ts1 adults raised at the non-permissive temperature have a greatly increased number of midgut enteroendocrine cells. Nl1N-ts1 mutants show as much as a fivefold increase in class I da neuron number. However, dendrite arborization is unaffected. Mutant brains from third instar larvae maintained at 29oC from larval hatching have fewer neuroblasts than normal. Only 1.1% of the neuroblasts are dividing in the mutant brains, compared to 18% in wild type. 24 hours at the restrictive temperature is sufficient to disrupt anterior morphogenesis in Nl1N-ts1 mutant egg chambers. This results in cup-shaped eggshells with open anterior and short, wide dorsal appendages. Nurse cell dumping is incomplete. Examination of these stage 10 Nl1N-ts1 mutant egg chambers, following a 24 hour restrictive temperature shift, shows that follicle cell organization in the region of the nurse cell-oocyte boundary is affected. The boundary between the squamous follicle cells and the columnar follicle cells is sometimes normally placed over the nurse cell-oocyte boundary and sometimes aberrantly placed over the nurse cells. In both cases, no centripetally migrating follicle cells are observed. Extra R8 and other neurons differentiate and no second mitotic wave occurs in N[l1N-ts1] eye discs at the restrictive temperature. At 18oC, the dorsoventral interface of Nl1N-ts1 wing discs is normal or subtly disturbed, while at 29oC the dorsoventral interface is grossly distubed. The F-actin organization and cellular morphology usually observed along the dorsoventral interface is eliminated. Nl1N-ts1 females raised at the restrictive temperature show severe border cell migration defects in a significant number of egg chambers. There is an increase in the number of R8 neurons in the eye disc of N[l1N-ts1] animals raised at non-permissive temperatures. Nl1N-ts1 animals raised at 18oC until 14 hours after puparium formation (APF) and then switched to 32oC for 6 hours show a significant reduction in cell death in the pupal retina compared to wild type (and a corresponding excess in the number of cells in the retina). There is a block in differentiation of the primary pigment cells in these animals, a failure of interommatidial cells to reorganise and improper ommatidia alignment. At 24 hours after puparium formation, the numbers of founder myoblasts in the dorsal or lateral segments of the abdomen of Nl1N-ts1 animals switched to the non-permissive temperature 2, 4, 6 or 8 hours earlier are normal. Female flies heterozygous for Nl1N-ts1 and reared at 25 oC show thickened wing vein L3 and duplicated anterior and posterior scutellar macrochaetae. Nl1N-ts1 mutants, which are shifted to the restrictive temperature (310C) between 6 and 8 hours after fertilization (stage 11), show an increase in the number of lymph-gland progenitors, cardioblasts and pericardial nephrocytes that develop from the cardiogenic mesoderm. Stage 15 Nl1N-ts1 mutant embryos that have been reared at the restrictive temperature 8-10 hours after fertilization show an increase in the number of cardioblasts and a concomitant loss of pericardial and lymph-gland cells. Mutant males tested at the non-permissive temperature, exhibit a loss of long term memory in courtship conditioning and Pavlovian olfactory conditioning tests. Short term memory remains normal. Nl1N-ts1/Df(1)N-81k1 embryos have excess cardioblasts, which form three to four poorly organised rows (in wild-type embryos they form two cell rows). The number of pericardial cells is relatively normal. Nl1N-ts1 embryos raised at 30oC have a weak excess cardioblast phenotype. 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. Mutant animals exhibit fusion and truncation of tarsomeres. Shifting Nl1N-ts1 mutant larvae to the nonpermissive temperature in mid-late-L1 results in eye-antennal discs that are reduced in size. When Nl1N-ts1 animals are pulsed at 32oC from 10 to 16 hours APF, a significant number of external sensory structures are seen on the antennal surface. The diameter of fascicles in antennal segment 3 are also increased. 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". All macrochaetae are absent from the heads of Nl1N-ts1 flies raised at 29oC. When maintained at 18[o]C (the permissive temperature) N[l1N-ts1] mutant late third instar (wandering) larvae have wild-type numbers of circulating plasmatocytes and crystal cells. However, when N[l1N-ts1] mutant larvae are shifted to 29[o]C (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 prophenoloxidase 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 N[l1N-ts1] raised at 29[o]C compared to wild-type, or to N[l1N-ts1] larvae raised at 18[o]C assayed 72-96 hours after parasitization. In mutants at the non-permissive temperature, overspecification of R cells is seen, as well loss of cone cell specification. Nl1N-ts1 flies show a wild-type morphology, including a normal array of neurosensory bristles. 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. 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. 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. The retina of flies that have received an 8 hour heat shock pulse during the pupal stage (either at 42 hours after puparium formation (APF) if raised at 18[o]C or at 21 hours APF if raised at 25[o]C) contains additional 2[o]/3[o] pigment cells. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. Eye discs maintained at the restrictive temperature contain extra R8 photoreceptor cells. 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. 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. 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. 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. 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. 84% of the egg chambers of homozygous females maintained at the restrictive temperature for 64 hours are 'compound egg chambers'. 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. 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. Homozygous clones exhibit a strong neurogenic phenotype, all bristles at the border of the clone are mutant. After shifting to the restrictive temperature for 7 hours a region of extensive neural hypertrophy is left behind as the morphogenetic furrow advances. Misappropriate development of stalk cells, stalk cells are not established no egg chambers fail to separate. 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. Temperature shifts reveal that neurogenic gene function is continuously required throughout SNS morphogenesis. 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}. Bristle multiplication phenotype on the thorax. 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. 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. Wing and wing pouch are reduced. 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. 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. Temperature-sensitive allele. Aberrant bristles are produced on the labellum if pupae are exposed to pulses of the restrictive temperature. 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. 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. 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). Epistatic to sgg32. 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. 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. 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. 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. 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. 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. 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. 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. Weak embryonic neurogenic phenotype at 29oC. 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. 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). | |||
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External Data
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| Linkouts | |||
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Interactions
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Phenotypic Class
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| Enhanced by | |||
Statement Reference Nl1N-ts1, trio123.4/trio[+] has neuroanatomy defective | heat sensitive phenotype, enhanceable by Scer\GAL4elav-C155/trioScer\UAS.cBa Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, enhanceable by Scer\GAL460/Rac1N17.Scer\UAS Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, enhanceable by Scer\GAL460/Rac1V12.Scer\UAS Nl1N-ts1 has neuroanatomy defective | recessive phenotype, enhanceable by cpbScer\UAS.cWa/Scer\GAL415J2 Nl1N-ts1 has neuroanatomy defective | recessive phenotype, enhanceable by Scer\GAL415J2/DlΔIC.Scer\UAS Nl1N-ts1 has neuroanatomy defective | recessive phenotype, enhanceable by Scer\GAL415J2/trioGEF1.Scer\UAS.T:Hsap\MYC Nl1N-ts1 has neuroanatomy defective | recessive phenotype, enhanceable by Scer\GAL415J2/Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP Nl1N-ts1 has visible | recessive | heat sensitive phenotype, enhanceable by E(spl)mγ-HLHScer\UAS.cLa/Scer\GAL432B Nl1N-ts1 has visible | recessive | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)m7-HLHScer\UAS.cdCa Nl1N-ts1 has visible | recessive | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)m8-HLHScer\UAS.cNa Nl1N-ts1 has visible | recessive | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)mβ-HLHScer\UAS.cdCa Nl1N-ts1 has visible | recessive | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)mδ-HLHScer\UAS.cdCa | |||
| NOT Enhanced by | |||
Statement Reference Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-enhanceable by Rho1V14.Scer\UAS/Scer\GAL460 Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-enhanceable by Scer\GAL460/Cdc42V12.Scer\UAS Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-enhanceable by Scer\GAL460/Rac1Scer\UAS.cLa Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-enhanceable by Scer\GAL4elav-C155/Cdc42N17.Scer\UAS Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-enhanceable by Scer\GAL4elav-C155/Rho1N19.Scer\UAS | |||
| Suppressed by | |||
Statement Reference Nl1N-ts1, trio123.4/trio[+] has neuroanatomy defective | heat sensitive phenotype, suppressible by Scer\GAL4elav-C155/trioGEF1mu.Scer\UAS Nl1N-ts1 has decreased cell number | larval stage | temperature conditional phenotype, suppressible | somatic clone by dpnScer\UAS.cSa/Scer\GAL4Scer\FRT.Act5C Nl1N-ts1 has lethal | pupal stage | heat sensitive phenotype, suppressible by insvunspecified/insvunspecified Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, suppressible by Rac2Δ/Mtl[+]/MtlΔ/Rac2[+]/Rac1J10/Rac1[+] Nl1N-ts1 has neuroanatomy defective | larval stage | temperature conditional phenotype, suppressible | somatic clone by dpnScer\UAS.cSa/Scer\GAL4Scer\FRT.Act5C Nl1N-ts1 has neuroanatomy defective | recessive phenotype, suppressible by enaScer\UAS.T:Avic\GFP/Scer\GAL415J2 Nl1N-ts1 has neuroanatomy defective | recessive phenotype, suppressible by Scer\GAL415J2/Rac1N17.Scer\UAS Nl1N-ts1 has neuroanatomy defective | recessive phenotype, suppressible by Su(H)Scer\UAS.T:Hsap\MYC,T:Hsim\VP16/Scer\GAL4repo-M1B Nl1N-ts1 has visible | recessive | heat sensitive phenotype, suppressible by E(spl)mγ-HLHScer\UAS.cLa/Scer\GAL432B Nl1N-ts1 has visible | recessive | heat sensitive phenotype, suppressible by Scer\GAL432B/E(spl)mδ-HLHScer\UAS.cdCa | |||
| NOT suppressed by | |||
Statement Reference Nl1N-ts1, trio123.4/trio[+] has neuroanatomy defective | heat sensitive phenotype, non-suppressible by Scer\GAL4elav-C155/trioGEF1mu.Scer\UAS Nl1N-ts1 has lethal | pupal stage | heat sensitive phenotype, non-suppressible by insvunspecified/insv[+] Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-suppressible by Rho1rev220/Rho1[+] Nl1N-ts1 has neuroanatomy defective | recessive phenotype, non-suppressible by Scer\GAL415J2/Su(H)Scer\UAS.T:Hsap\MYC,T:Hsim\VP16 | |||
| Enhancer of | |||
Statement Reference | |||
| Suppressor of | |||
Statement Reference Nl1N-ts1 is a suppressor | heat sensitive of visible phenotype of Dip3C00008, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF | |||
| Other | |||
Statement Reference | |||
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Phenotype Manifest In
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| Enhanced by | |||
Statement Reference Nl1N-ts1, trio123.4/trio[+] has intersegmental nerve | heat sensitive phenotype, enhanceable by Scer\GAL4elav-C155/trioScer\UAS.cBa Nl1N-ts1, trio123.4/trio[+] has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, enhanceable by Scer\GAL4elav-C155/trioScer\UAS.cBa Nl1N-ts1 has anterior scutellar bristle phenotype, enhanceable by Scer\GAL4dpp.blk1/Hs3st-BdsRNA.IR.Scer\UAS Nl1N-ts1 has embryonic/larval dorsal branch phenotype, enhanceable by dppScer\UAS.cRa/Scer\GAL4btl.PS Nl1N-ts1 has embryonic/larval dorsal branch phenotype, enhanceable by Scer\GAL4btl.PS/tkvQ253D.Scer\UAS.cNb Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, enhanceable by Scer\GAL460/Rac1N17.Scer\UAS Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, enhanceable by Scer\GAL460/Rac1V12.Scer\UAS Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, enhanceable by Scer\GAL4unspecified/AblScer\UAS.cFa Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, enhanceable by Scer\GAL460/Rac1N17.Scer\UAS Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, enhanceable by Scer\GAL460/Rac1V12.Scer\UAS Nl1N-ts1 has pioneer neuron phenotype, enhanceable by Scer\GAL415J2/Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP Nl1N-ts1 has posterior scutellar bristle phenotype, enhanceable by Scer\GAL4dpp.blk1/Hs3st-BdsRNA.IR.Scer\UAS | |||
| NOT Enhanced by | |||
Statement Reference Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Rho1V14.Scer\UAS/Scer\GAL460 Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Scer\GAL460/Cdc42V12.Scer\UAS Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Scer\GAL460/Rac1Scer\UAS.cLa Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Scer\GAL4elav-C155/Cdc42N17.Scer\UAS Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Scer\GAL4elav-C155/Rho1N19.Scer\UAS Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, non-enhanceable by Rho1V14.Scer\UAS/Scer\GAL460 Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, non-enhanceable by Scer\GAL460/Cdc42V12.Scer\UAS Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, non-enhanceable by Scer\GAL460/Rac1Scer\UAS.cLa Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, non-enhanceable by Scer\GAL4elav-C155/Cdc42N17.Scer\UAS Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, non-enhanceable by Scer\GAL4elav-C155/Rho1N19.Scer\UAS | |||
| Suppressed by | |||
Statement Reference Nl1N-ts1, trio123.4/trio[+] has intersegmental nerve | heat sensitive phenotype, suppressible by Scer\GAL4elav-C155/trioGEF2mu.Scer\UAS Nl1N-ts1, trio123.4/trio[+] has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, suppressible by Scer\GAL4elav-C155/trioGEF2mu.Scer\UAS Nl1N-ts1, trio123.4/trio[+] has segmental nerve branch SNa of A1-7 | heat sensitive phenotype, suppressible by Scer\GAL4elav-C155/trioGEF2mu.Scer\UAS Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, suppressible | partially by Abl1/Abl[+] Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, suppressible | partially by Df(3L)st-j7 Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, suppressible | partially by Nrt[+]/NrtM54 Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, suppressible | partially by NrtM54/Abl1 Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, suppressible | partially by trio123.4/trio[+] Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, suppressible by Rac2Δ/MtlΔ/Rac1J10/Rac1[+] Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, suppressible by Rac2Δ/Mtl[+]/MtlΔ/Rac2[+]/Rac1J10/Rac1[+] Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, suppressible by trio123.4/trio[+] Nl1N-ts1 has phenotype, suppressible by Su(H)hs.PS Nl1N-ts1 has pioneer neuron phenotype, suppressible by Su(H)Scer\UAS.T:Hsap\MYC,T:Hsim\VP16/Scer\GAL4repo-M1B Nl1N-ts1 has segmental nerve branch SNa of A1-7 | heat sensitive phenotype, suppressible by Rac2Δ/Mtl[+]/MtlΔ/Rac2[+]/Rac1J10/Rac1[+] Nl1N-ts1 has type II neuroblast | larval stage | temperature conditional phenotype, suppressible | somatic clone by dpnScer\UAS.cSa/Scer\GAL4Scer\FRT.Act5C Nl1N-ts1 has wing | heat sensitive phenotype, suppressible by Scer\GAL432B/E(spl)mδ-HLHScer\UAS.cdCa | |||
| NOT suppressed by | |||
Statement Reference Nl1N-ts1, trio123.4/trio[+] has intersegmental nerve | heat sensitive phenotype, non-suppressible by Scer\GAL4elav-C155/trioGEF1mu.Scer\UAS Nl1N-ts1, trio123.4/trio[+] has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, non-suppressible by Scer\GAL4elav-C155/trioGEF1mu.Scer\UAS Nl1N-ts1, trio123.4/trio[+] has segmental nerve branch SNa of A1-7 | heat sensitive phenotype, non-suppressible by Scer\GAL4elav-C155/trioGEF1mu.Scer\UAS Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-suppressible by Rho1rev220/Rho1[+] Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, non-suppressible by Cdc42[+]/Cdc424 Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, non-suppressible by Rho1rev220/Rho1[+] Nl1N-ts1 has mechanosensory sensory organ phenotype, non-suppressible by Scer\GAL4sca-537.4/Hsap\APLP2::Hsap\APPScer\UAS.T:Hsap\MYC Nl1N-ts1 has pioneer neuron phenotype, non-suppressible by Scer\GAL415J2/Su(H)Scer\UAS.T:Hsap\MYC,T:Hsim\VP16 Nl1N-ts1 has segmental nerve branch SNa of A1-7 | heat sensitive phenotype, non-suppressible by Cdc42[+]/Cdc424 Nl1N-ts1 has segmental nerve branch SNa of A1-7 | heat sensitive phenotype, non-suppressible by Rho1rev220/Rho1[+] | |||
| Enhancer of | |||
Statement Reference Nl1N-ts1 is an enhancer of embryonic/larval dorsal branch phenotype of Scer\GAL4btl.PS, dppScer\UAS.cRa Nl1N-ts1 is an enhancer of embryonic/larval dorsal branch phenotype of Scer\GAL4btl.PS, tkvQ253D.Scer\UAS.cNb | |||
| Suppressor of | |||
Statement Reference Nl1N-ts1 is a suppressor | heat sensitive of eye phenotype of Dip3C00008, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF Nl1N-ts1 is a suppressor | heat sensitive of ommatidium phenotype of Dip3C00008, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF Nl1N-ts1 is a suppressor | partially of basal cylinder phenotype of DlScer\UAS.cDa, Scer\GAL4ap-md544 Nl1N-ts1 is a suppressor of joint | supernumerary phenotype of TfAP-2Scer\UAS.cMa, Scer\GAL4ptc-559.1 Nl1N-ts1 is a suppressor of type II neuroblast | supernumerary phenotype of Scer\GAL41407, numbTS4D.Scer\UAS | |||
| Other | |||
Statement Reference Nl1N-ts1, l(2)glunspecified has eo neuron | cell non-autonomous | somatic clone | supernumerary phenotype Nl1N-ts1, l(2)glunspecified has thecogen cell | cell non-autonomous | somatic clone | supernumerary phenotype | |||
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Additional Comments
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Genetic Interactions
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Statement Reference The ectopic microchaetae seen on the notum in N[l1N-ts1] females raised at 22[o]C are suppressed by insv[23B].
The pupal lethality caused by N[l1N-ts1] at 25[o]C is suppressed by homozygosity for insv[unspecified].
The double-socketed sensory organs on the abdomen which are seen in insv[23B] adults are largely suppressed by N[l1N-ts1] at 25[o]C. Expression of Dl[ΔIC.Scer\UAS] under the control of Scer\GAL4[15J2] enhances the N[l1N-ts1] early axon phenotype.
The N[l1N-ts1] pioneer axon phenotype is strongly enhanced by heterozygosity for fra[2].
The N[l1N-ts1] pioneer axon phenotype is strongly enhanced by heterozygosity for fra[4].
The N[l1N-ts1], Df(1)NetAB[Δ] double mutant has a significantly higher frequency of longitudinal axon defects than either mutant by itself.
Expression of Su(H)[Scer\UAS.T:Hsap\MYC,T:Hsim\VP16] in glia under the control of Scer\GAL4[repo-M1B] suppresses the N[l1N-ts1] longitudinal pioneer axon phenotype.
Expression of Su(H)[Scer\UAS.T:Hsap\MYC,T:Hsim\VP16] in the pioneer neurons under the control of Scer\GAL4[15J2] fails to suppress the N[l1N-ts1] longitudinal pioneer axon phenotype.
Abl[4]/+ suppresses the mature stage 16 CNS axonal phenotype of N[l1N-ts1].
Expression of ena[Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[15J2] suppresses the early longitudinal axon phenotype of N[l1N-ts1].
Overexpression of cpb[Scer\UAS.cWa] under the control of Scer\GAL4[15J2] enhances the early longitudinal axon phenotype of N[l1N-ts1].
Overexpression of trio[GEF1.Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[15J2] enhances the early longitudinal axon phenotype of N[l1N-ts1].
Overexpression of Rac1[N17.Scer\UAS] under the control of Scer\GAL4[15J2] suppresses the early longitudinal axon phenotype of N[l1N-ts1]. Inhibition of N activity through N[l1N-ts1] suppresses numb[TS4D.Scer\UAS] induced ectopic neuroblast formation. The ectopic leg joint phenotype caused by expression of tal[Scer\UAS.cGa] under the control of Scer\GAL4[bab1-GAL4-U] is suppressed by N[l1N-ts1]/+ (at the restrictive temperature). Expressing dpn[Scer\UAS.cSa] in clones under the control of Scer\GAL4[Scer\FRT.Act5C] suppresses neuroblast loss seen when N[l1N-ts1] is shifted to the restrictive temperature from the first instar larval stage onwards. A trio[123.4] heterozygous background significantly restores the ability of ISNb axons to enter the ventrolateral muscle field in N[l1N-ts1] mutants. This suppression is reverted upon pan-neural expression of trio[Scer\UAS.cBa] under the control of Scer\GAL4[elav-C155].
Pan-neuronal expression of trio[GEF1mu.Scer\UAS] in a N[l1N-ts1]; trio[123.4]/+ background (under the control of Scer\GAL4[elav-C155]) does not restore the ability of ISNb axons to enter the ventrolateral muscle field.
Pan-neuronal expression of trio[GEF2mu.Scer\UAS] in a N[l1N-ts1]; trio[123.4]/+ background (under the control of Scer\GAL4[elav-C155]) restores the ability of ISNb axons to enter the ventrolateral muscle field.
Heterozygosity for Rac1[J10] Rac2[Δ] Mtl[Δ] suppresses the axonal defects found in N[l1N-ts1] mutants.
Heterozygosity for Cdc42[4] or Rho1[rev220] fails to suppress the axonal defects found in N[l1N-ts1] mutants.
Expression of a constitutively active form of Rac1, Rac1[V12.Scer\UAS] under the control of Scer\GAL4[60], significantly increases the occurrence of ISNb bypass in N[l1N-ts1] embryos.
Expression of Rac1[N17.Scer\UAS] under the control of Scer\GAL4[60], significantly increases the occurrence of ISNb bypass in N[l1N-ts1] embryos.
The ISNb bypass phenotype of N[l1N-ts1] mutant embryos is not significantly modulated by expression of Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[60].
The ISNb bypass phenotype of N[l1N-ts1] mutant embryos is not significantly modulated by expression of Cdc42[V12.Scer\UAS] (under the control of Scer\GAL4[60]) or Cdc42[N17.Scer\UAS] (under the control of Scer\GAL4[elav-C155]).
The ISNb bypass phenotype of N[l1N-ts1] mutant embryos is not significantly modulated by expression of Rho1[V14.Scer\UAS] (under the control of Scer\GAL4[60]) or Rho1[N19.Scer\UAS] (under the control of Scer\GAL4[elav-C155]). Homozygous seq[A41] clones in the thorax generated in N[l1N-ts1] animals grown at the restrictive temperature generate socket cells within the clone. The retinal disorganisation and interommatidial pigment cell death observed in Chc[4] mutant flies is suppressed in animals carrying a mutation in N[l1N-ts1] (when animals are grown at 18[o]C and then shifted to 31[o]C (once 40% through pupal development) for 6 hours). The smooth eye phenotype caused by expression of Dip3[C00008] under the control of Scer\GAL4[GMR.PF] is partially suppressed by N[l1N-ts1] at 29[o]C; more interommatidial bristles and a clear demarcation between the ommatidia are seen. A postorbital bristle multiple socket phenotype is not observed when N[l1N-ts1] is inactivated in a l(2)gd1[24] mutant eye clones N[l1N-ts1]; ft[8]/ft[422] double mutant larvae grown at restrictive temperature exhibit distal wing growth. Extra R8 and other neurons differentiate and no second mitotic wave occurs in N[l1N-ts1], Egfr[tsla] eye discs at the restrictive temperature. Hsap\APLP2::Hsap\APPScer\UAS.T:Hsap\MYC (driven by Scer\GAL4sca-537.4) does not suppress the Nl1N-ts1 bristle phenotype, but can induce transformations in wild-type mechanosensory organs in these animals. In ham1 homozygous clones induced in a Nl1N-ts1 background at the restrictive temperature, all external sensory organs develop a 1 trichogen/multiple tormogen phenotype, compared to ham1 homozygous clones induced in a wild-type background, where external sensory organs develop a 2 trichogen/multiple tormogen phenotype. When l(2)glunspecified clones are made in Nl1N-ts1/Df pupae that are moved to the restrictive temperature, loss of external cell are seen within and outside l(2)glunspecified clones. The macrochaetae phenotype exhibited by the heads of Nl1N-ts1 flies at 29oC is unaffected by somatic clones of α-Adaptinear4. WASp1/Df(3R)3450 Nl1N-ts1 flies show an enhancement of the WASp1/Df(3R)3450 bristle loss phenotype; the flies lack practically all bristles on regions of the cuticle such as the thorax. The addition of Nl1N-ts1 (with an associated growth at the restrictive temperature of 29oC) to DlScer\UAS.cDa/Scer\GAL4ap-md544 flies completely restores the wild-type pattern of leg segmentation. Nl1N-ts1 ovarioles expressing DlScer\UAS.cDa under the control of Scer\GAL4hs.PB have the same phenotype as Nl1N-ts1 ovarioles; no stalk cells are produced. The wing phenotype of flies shifted to the non-permissive temperature at the early third larval instar stage (72-84 hours after egg laying) is enhanced by E(spl)Scer\UAS.cNa, HLHm7Scer\UAS.cdCa, HLHmγScer\UAS.cLa, HLHmδScer\UAS.cdCa or HLHmβScer\UAS.cdCa expressed under the control of Scer\GAL432B. The wing phenotype of hemizygous flies shifted to the non-permissive temperature at the mid third larval instar stage (96-108 hours after egg laying) is suppressed by HLHmγScer\UAS.cLa or HLHmδScer\UAS.cdCa expressed under the control of Scer\GAL432B, while expression of E(spl)Scer\UAS.cNa, HLHm7Scer\UAS.cdCa or HLHmβScer\UAS.cdCa under the control of Scer\GAL432B has no effect on the phenotype. At 18oC, enhances lethality of hemizygous Abl1 or Abl2 such that less than 1.5% of flies survive. Affected embryos do not show a neurogenic or antimyogenic phenotype. The gross morphology of the embryos is normal but they show axonal defects in all axon tracts known to require N function: CNS longitudinal tracts between neuromeres and the lateral portion of the ISN. Defects are evident from stage 13, in the combined MP fascicle. The nerve frays and stalls precisely as it attempts to grow along the trachea. The LG5 glial cell is present. Neurons aCC MP1 pCC dMP2 and vMP2 are all present. Pioneer neuron identity is unaffected (as assayed by ftz, eve, odd, Fas2 and pros expression). Transheterozygotes with toc alleles exhibit ovary defects. Removal of N activity can suppress the P{sev-wg.C} phenotype, almost complete loss of interommatidial bristles. | |||
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Xenogenetic Interactions
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Statement Reference Expression of Zzzz\actA[FP4mito.Scer\UAS.T:Avic\GFP-EGFP] under the control of Scer\GAL4[15J2] enhances the early longitudinal axon phenotype of N[l1N-ts1]. Hsap\APLP2::Hsap\APPScer\UAS.T:Hsap\MYC (driven by Scer\GAL4sca-537.4) does not suppress the Nl1N-ts1 bristle phenotype, but can induce transformations in wild-type mechanosensory organs in these animals. | |||
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Complementation & Rescue Data
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| Complements | |||
| Fails to complement | |||
| Rescued by | |||
| Partially rescued by | |||
| Not rescued by | Nl1N-ts1 is not rescued by NΔEGF1-18.hs | ||
| Comments | Expression of N[Scer\UAS.cUa] under the control of Scer\GAL4[repo-M1B] efficiently rescues the early axon phenotype of N[l1N-ts1] and restores restores the continuity of the neuronal meshwork.
Expression of N[Scer\UAS.cUa] under the control of Scer\GAL4[htl.PM] efficiently rescues the early axon phenotype of N[l1N-ts1].
Expression of N[Scer\UAS.cUa] under the control of Scer\GAL4[15J2] efficiently rescues the early axon phenotype of N[l1N-ts1].
Expression of N[FLNΔ10-12.Scer\UAS] under the control of Scer\GAL4[15J2] fails to rescue the N[l1N-ts1] axon phenotype.
Expression of N[1893-2155.Scer\UAS] in pioneer neurons under the control of Scer\GAL4[15J2] partially rescues axon extension in N[l1N-ts1] mutant embryos. The defects in axons entering the optic lobe seen in Nl1N-ts1 larvae lacking N+ activity are not rescued by NScer\UAS.cBa expressed under the control of Scer\GAL4ato.3.6. Failure to complement is at 29oC, complementation is at 18oC. | ||
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Stocks
( 2 ) | |||
| Bloomington | |||
| Kyoto | |||
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Notes on Origin
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| Discoverer | Shellenbarger. | ||
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Comments
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Used to determine phenocritical periods for N in development of neuroblasts, sensillum precursors, sensory neurons, peripheral glial cells, oenocytes, optic lobe, somatogastric nervous system, salivary gland, foregut, Malpighian tubules, trachea, endoderm, larval midgut, somatic musculature, cardioblasts, pericardial cells, peritracheal and periligament cells and dorsomedial cells. Weak N allele. | |||
 External Crossreferences & Linkouts
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Synonyms & Secondary IDs
( 13 ) | |||
| Reported As | |||
| Symbol Synonym | l(1)Nts1 l(1)Nts Nl1N-ts1 Nl1-Nts1 Nts1 (Dobens et al., 2005, Micchelli and Perrimon, 2006, Grzeschik and Knust, 2005, Aigouy et al., 2004, Mandal et al., 2004, Merdes et al., 2004, Dutta et al., 2004, Kenyon et al., 2003, Moore et al., 2004, del Alamo Rodriguez et al., 2004, Chou and Chien, 2002, Crowner et al., 2003, Rawls and Wolff, 2003, Duvic et al., 2002, Lebestky et al., 2003, Tang and Sun, 2002, Tsuda et al., 2002, Barolo et al., 2002, Pickup et al., 2002, Ramain et al., 2001, Mishra et al., 2001, van de Bor and Giangrande, 2001, Udolph et al., 2001, Furriols and Bray, 2001, Ben-Yaacov et al., 2001, Barolo et al., 2000, Flores et al., 2000, Zhao et al., 2000, Wesley and Saez, 2000, Tomlinson and Struhl, 1999, Periz and Fortini, 1999, Micchelli and Blair, 1999, Ye and Fortini, 1999, Steneberg et al., 1999, Rangarajan et al., 1999, Ikeya and Hayashi, 1999, zur Lage and Jarman, 1999, Wai et al., 1999, Bishop et al., 1999, Llimargas, 1999, Ligoxygakis et al., 1999, Larkin et al., 1999, Ye et al., 1999, Haag et al., 1999, Fanto and Mlodzik, 1999, Lesokhin et al., 1999, Sun et al., 1998, Baker and Yu, 1998, Fuerstenberg and Giniger, 1998, Gonzalez-Reyes and St. Johnston, 1998, Buescher et al., 1998, Martinez Arias, 1998, Anant et al., 1998, Giniger, 1998, Seugnet et al., 1997, Menne et al., 1997, Grammont et al., 1997, Jackson and Blochlinger, 1997, Micchelli et al., 1997, Baker and Yu, 1997, Reddy et al., 1997, Dokucu et al., 1996, Goode et al., 1996, Cadigan and Nusse, 1996, Baker et al., 1996, de Celis et al., 1996, Schweisguth et al., 1996, Lee et al., 1996, Zaffran et al., 1995, Heitzler et al., 1996, Hartenstein et al., 1996, Diaz-Benjumea and Cohen, 1995, Rulifson and Blair, 1995, Jennings et al., 1995, Baker and Zitron, 1995, Muskavitch, 1994, Li et al., 1994, Clark et al., 1994, Fortini and Artavanis-Tsakonas, 1994, Couso and Martinez Arias, 1994, Menne and Klambt, 1994, Cummings and Cronmiller, 1994, Coyle-Thompson and Banerjee, 1993, Dickson and Hafen, 1993, Skaer, 1993, Green et al., 1993, Bodmer et al., 1993, Heitzler and Simpson, 1993, Xu et al., 1992, Hartenstein et al., 1992, Woods and Bryant, 1992, Ruohola et al., 1991, Heitzler and Simpson, 1991, Baker et al., 1990, Hartenstein and Posakony, 1990, Cagan and Ready, 1989, Dietrich and Campos-Ortega, 1984, Lehmann et al., 1983, Bernard et al., 2006, Edenfeld et al., 2007, Apitz et al., 2005, Ward et al., 2006, Okegbe and DiNardo, 2011, Song et al., 2007, Peng et al., 2012, Eun et al., 2008, Bernard et al., 2009, Rebeiz et al., 2011, Gorski et al., 2000, Zhang et al., 2005, Peralta et al., 2009, Song and Giniger, 2011, Kuzina et al., 2011) Nts-1 Nts (Ghabrial and Krasnow, 2006, Micchelli and Perrimon, 2006, Ohlstein and Spradling, 2006, Major and Irvine, 2005, Bajpai et al., 2004, Kumar et al., 2003, Berdnik et al., 2002, Orgogozo et al., 2002, del Alamo Rodriguez et al., 2002, Rohrbaugh et al., 2002, Frankfort and Mardon, 2002, Pi et al., 2001, Cooper, 2000, Culi et al., 2001, Cooper and Bray, 2000, Dobens and Raftery, 2000, Jordan et al., 2000, Hassan et al., 2000, Micchelli and Blair, 1999, Chao and Nagoshi, 1999, zur Lage and Jarman, 1999, Simpson et al., 1999, Chen and Chien, 1999, Nagaraj et al., 1999, Cooper and Bray, 1999, Culi and Modolell, 1998, Majumdar et al., 1997, Larkin et al., 1996, Guo et al., 1996, Ma et al., 1996, Doherty et al., 1996, Couso et al., 1995, Jan and Jan, 1994, Costello, 1994, Ray and Rodrigues, 1994, Almeida and Bray, 2005, Parrish et al., 2006, Sato and Tomlinson, 2007, Kamimura et al., 2004, Kamimura et al., 2004, Lubensky et al., 2011, San-Juán and Baonza, 2011, Firth and Baker, 2005, Duan et al., 2011, Andrews et al., 2009, Bhattacharya and Baker, 2009, Duong et al., 2008, Jaiswal et al., 2006, Wang et al., 2008, Ouyang et al., 2011, Pueyo and Couso, 2011) Notchts1 notchts Notchts Nts1 ts1 | ||
| Name Synonym | Notchts | ||
| Secondary FlyBase IDs | |||
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References
( 191 ) | |||
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Recent research papers ( 12 ) | |||
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Recent reviews (0)
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| All reviews listed in FlyBase were published before 2011 | |||