Open Close
General Information
Symbol
Dmel\Nl1N-ts1
Species
D. melanogaster
Name
FlyBase ID
FBal0012887
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Nts1, Nts, Notchts1, Nts-1, notchts, l(1)Nts1, l(1)Nts
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:
G3166443A
Reported nucleotide change:
G4556A
Amino acid change:
G1272D | N-PA; G1272D | N-PB
Reported amino acid change:
G1272D
Comment:
Position of mutation on reference sequence inferred by FlyBase curator based on author statement.
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Amino acid replacement: G1272D.
Amino acid replacement: G1272D. Residue G1272 is within the 32nd EGF-like repeat.
Missense mutation in the extracellular domain.
Amino acid replacement: G1272D. G1272 falls in EGF repeat number 32.
Nucleotide substitution: G4556A. Amino acid replacement: G1272D. G1272D coordinates according to FBrf0042040. This change is within the 32nd EGF-like repeat.
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
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
Detailed Description
Statement
Reference
The legs of Nl1N-ts1 mutants shifted to the permissive temperature at the third instar larval stage show a complete absence of tarsal joints.
Nl1N-ts1 mutant lymph glands in third instar larvae do not exhibit a difference in lamellocyte differentiation and lobe dispersal in response to L. boulardi infection, as compared to controls.
Mutant pupae placed at a semi-permissive temperature at the time of division of pI (sensory organ precursor) cells in the notum show 7.3% pIIa-to-pIIb cell fate transformation.
Nl1N-ts1 flies maintained at the restrictive temperature during all of pupation show clustering of neighbouring axons in the medulla and a significant increase in the number of medulla axons compared to wild type. Temperature shift experiments indicate that the the temperature sensitive period is between 24 and 60 hours after puparium formation.
Nl1N-ts1 embryos kept at 29 degrees celsius during embryonic stages 8-11 (and 22 degrees celsius at other times) have no difference in number, size and position of mushroom body neuroblasts, but have increased number of other brain neuroblasts compared to controls, when analysed at stage 17.
Nl1N-ts1 animals raised at the restrictive temperature from 12 hours after puparium formation onwards and expressing NScer\UAS.cUa under the control of Scer\GAL4neur-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 Nl1N-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, Nl1N-ts1 animals show pupal lethality.
Mature longitudinal axon tracts of homozygous Nl1N-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 Nl1N-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 NdsRNA.Scer\UAS.cUa under the control of Scer\GAL4repo-M1B enhances the Nl1N-ts1 early axon phenotype. Nl1N-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 Nl1N-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 Nl1N-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 Nl1N-ts1 is shifted to the restrictive temperature from the first instar larval stage onwards.
Nl1N-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 Nl1N-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.
Nl1N-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.
Nl1N-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 Nl1N-ts1 during second instar larval stage (controlled by shifting Nl1N-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 Nl1N-ts1 raised at permissive temperatures show normal postorbital bristle morphology. When Nl1N-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 Nl1N-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 Nl1N-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 Nl1N-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.
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.
Mutant animals exhibit fusion and truncation of tarsomeres.
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) 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 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 Nl1N-ts1 raised at 29[o]C compared to wild-type, or to Nl1N-ts1 larvae raised at 18[o]C assayed 72-96 hours after parasitization.
N55e11/Nl1N-ts1 flies form ectopic abdominal ventral multidendritic neurons and pI external sensory organ precursor cells, even when raised at 19oC.
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.
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.
Nl1N-ts1 flies raised at 18[o]C do not exhibit a developmental susceptibility to early death. Females homozygous for Nl1N-ts1 lose their ability to fly after a shift to 29[o]C. This loss of flight appears to be an early stage in the progression of a lethal neurological impairment, since Nl1N-ts1 flies typically lost their ability to fly prior to their death. These flies also display an impairment in negative geotaxis and righting reflexes in flies of both genders, within a few days of a shift to 29[o]C. No evidence of neurodegeneration, including apoptosis or vacuolization is found in these flies.
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.
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/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.
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.
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.
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.
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.
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/N55e11 wing discs show a reduction in the size of the pouch.
Nl1N-ts1/Nfa-g62 flies show a temperature sensitive roughening of the eye.
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.
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.
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.
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.
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.
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.
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.
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).
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Nl1N-ts1 has neuroanatomy defective | recessive phenotype, enhanceable by fra2/fra[+]
Nl1N-ts1 has neuroanatomy defective | recessive phenotype, enhanceable by fra4/fra[+]
Nl1N-ts1, trio123.4/trio[+] has neuroanatomy defective | heat sensitive phenotype, enhanceable by Scer\GAL4elav-C155/trioUAS.cBa
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, enhanceable by Scer\GAL460/Rac1V12.UAS
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, enhanceable by Scer\GAL460/Rac1N17.UAS
Nl1N-ts1 has visible | recessive | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)mβ-HLHUAS.cdCa
Nl1N-ts1 has visible | recessive | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)m8-HLHUAS.cNa
Nl1N-ts1 has visible | recessive | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)m7-HLHUAS.cdCa
Nl1N-ts1 has visible | recessive | heat sensitive phenotype, enhanceable by E(spl)mγ-HLHUAS.cLa/Scer\GAL432B
Nl1N-ts1 has visible | recessive | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)mδ-HLHUAS.cdCa
NOT Enhanced by
Statement
Reference
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-enhanceable by Scer\GAL460/Rac1UAS.cLa
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-enhanceable by Scer\GAL460/Cdc42V12.UAS
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-enhanceable by Scer\GAL4elav-C155/Cdc42N17.UAS
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-enhanceable by Rho1V14.UAS/Scer\GAL460
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-enhanceable by Scer\GAL4elav-C155/Rho1N19.UAS
Suppressed by
Statement
Reference
Nl1N-ts1 has visible phenotype, suppressible by insv23B
Nl1N-ts1 has lethal | pupal stage | heat sensitive phenotype, suppressible by insvunspecified/insvunspecified
Nl1N-ts1 has neuroanatomy defective | recessive phenotype, suppressible by Abl4/Abl[+]
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, suppressible by trio123.4/trio[+]
Nl1N-ts1, trio123.4/trio[+] has neuroanatomy defective | heat sensitive phenotype, suppressible by Scer\GAL4elav-C155/trioGEF1mu.UAS
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, suppressible by Rac2Δ/Mtl[+]/MtlΔ/Rac2[+]/Rac1J10/Rac1[+]
Nl1N-ts1 has visible | heat sensitive phenotype, suppressible | partially by CtBP[+]/CtBP87De-10
Nl1N-ts1 has visible | heat sensitive phenotype, suppressible | partially by groE73/gro[+]
Nl1N-ts1 has visible | heat sensitive phenotype, suppressible by H[+]/HE31
Nl1N-ts1 has visible | recessive | heat sensitive phenotype, suppressible by E(spl)mγ-HLHUAS.cLa/Scer\GAL432B
Nl1N-ts1 has visible | recessive | heat sensitive phenotype, suppressible by Scer\GAL432B/E(spl)mδ-HLHUAS.cdCa
NOT suppressed by
Statement
Reference
Nl1N-ts1 has lethal | pupal stage | heat sensitive phenotype, non-suppressible by insvunspecified/insv[+]
Nl1N-ts1, trio123.4/trio[+] has neuroanatomy defective | heat sensitive phenotype, non-suppressible by Scer\GAL4elav-C155/trioGEF1mu.UAS
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-suppressible by Cdc42[+]/Cdc424
Nl1N-ts1 has neuroanatomy defective | heat sensitive phenotype, non-suppressible by Rho1rev220/Rho1[+]
Enhancer of
Statement
Reference
Nl1N-ts1/N[+] is an enhancer of visible | somatic clone phenotype of emc1
Nl1N-ts1 is an enhancer of lethal phenotype of Abl2/Df(3L)st-j7
Nl1N-ts1 is an enhancer of lethal phenotype of Abl1/Df(3L)st-j7
Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
Nl1N-ts1 has pioneer neuron phenotype, enhanceable by fra2/fra[+]
Nl1N-ts1 has pioneer neuron phenotype, enhanceable by fra4/fra[+]
Nl1N-ts1, trio123.4/trio[+] has intersegmental nerve | heat sensitive phenotype, enhanceable by Scer\GAL4elav-C155/trioUAS.cBa
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, enhanceable by Scer\GAL460/Rac1V12.UAS
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, enhanceable by Scer\GAL460/Rac1N17.UAS
Nl1N-ts1 has cardioblast | supernumerary phenotype, enhanceable by lqf[+]/lqfARI
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, enhanceable by Scer\GAL4unspecified/AblUAS.cFa
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, enhanceable by enaGC1
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, enhanceable by enaGC5
Nl1N-ts1 has wing | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)mβ-HLHUAS.cdCa
Nl1N-ts1 has wing | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)m8-HLHUAS.cNa
Nl1N-ts1 has wing | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)m7-HLHUAS.cdCa
Nl1N-ts1 has wing | heat sensitive phenotype, enhanceable by E(spl)mγ-HLHUAS.cLa/Scer\GAL432B
Nl1N-ts1 has wing | heat sensitive phenotype, enhanceable by Scer\GAL432B/E(spl)mδ-HLHUAS.cdCa
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAI1
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAI1
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAAF1
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAAF1
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAA2
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAA2
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAD3
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAD3
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAP2
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAP2
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAS4
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAS4
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAAC1
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAAC1
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAAG2
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAAG2
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAAH2
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAAH2
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAAH7
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAAH7
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAAI5
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAAI5
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAAK1
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAAK1
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAAO5
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAAO5
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAAS2
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAAS2
Nl1N-ts1 has eye phenotype, enhanceable by Ca-P60A[+]/SERCAAT1
Nl1N-ts1 has lens phenotype, enhanceable by Ca-P60A[+]/SERCAAT1
NOT Enhanced by
Statement
Reference
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Scer\GAL460/Rac1UAS.cLa
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Scer\GAL460/Cdc42V12.UAS
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Scer\GAL4elav-C155/Cdc42N17.UAS
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Rho1V14.UAS/Scer\GAL460
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Scer\GAL4elav-C155/Rho1N19.UAS
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by Su(H)2
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-enhanceable by mam23
Suppressed by
Statement
Reference
Nl1N-ts1 has microchaeta | supernumerary phenotype, suppressible by insv23B
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, suppressible by trio123.4/trio[+]
Nl1N-ts1 has intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype, suppressible by trio123.4/trio[+]
Nl1N-ts1, trio123.4/trio[+] has intersegmental nerve | heat sensitive phenotype, suppressible by Scer\GAL4elav-C155/trioGEF2mu.UAS
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 segmental nerve branch SNa of A1-7 | heat sensitive phenotype, suppressible by Rac2Δ/Mtl[+]/MtlΔ/Rac2[+]/Rac1J10/Rac1[+]
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, suppressible | partially by trio123.4/trio[+]
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, suppressible | partially by NrtM54/Abl1
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 Abl1/Abl[+]
Nl1N-ts1 has chaeta | heat sensitive phenotype, suppressible | partially by CtBP[+]/CtBP87De-10
Nl1N-ts1 has chaeta | heat sensitive phenotype, suppressible | partially by groE73/gro[+]
Nl1N-ts1 has chaeta | heat sensitive phenotype, suppressible by H[+]/HE31
Nl1N-ts1 has wing | heat sensitive phenotype, suppressible by E(spl)mγ-HLHUAS.cLa/Scer\GAL432B
Nl1N-ts1 has wing | heat sensitive phenotype, suppressible by Scer\GAL432B/E(spl)mδ-HLHUAS.cdCa
Nl1N-ts1 has egg chamber phenotype, suppressible by ct[+]/ctC145
Nl1N-ts1 has egg chamber phenotype, suppressible by ct[+]/ctdb10
Nl1N-ts1 has phenotype, suppressible by Su(H)hs.PS
NOT suppressed by
Statement
Reference
Nl1N-ts1, trio123.4/trio[+] has intersegmental nerve | heat sensitive phenotype, non-suppressible by Scer\GAL4elav-C155/trioGEF1mu.UAS
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-suppressible by Cdc42[+]/Cdc424
Nl1N-ts1 has intersegmental nerve branch ISNb 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 Cdc42[+]/Cdc424
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 Rho1rev220/Rho1[+]
Nl1N-ts1 has segmental nerve branch SNa of A1-7 | heat sensitive phenotype, non-suppressible by Rho1rev220/Rho1[+]
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-suppressible by Su(H)2
Nl1N-ts1 has intersegmental nerve | heat sensitive phenotype, non-suppressible by mam23
Nl1N-ts1 has macrochaeta | heat sensitive phenotype, non-suppressible | somatic clone by AP-2αear4
Enhancer of
Statement
Reference
Nl1N-ts1 is an enhancer of adult thorax & microchaeta phenotype of Df(3R)3450/WASp1
Nl1N-ts1/N[+] is an enhancer of wing vein | somatic clone phenotype of emc1
Nl1N-ts1 is an enhancer of phenotype of gl3
Suppressor of
Statement
Reference
Nl1N-ts1 is a suppressor | partially of tormogen cell | ectopic phenotype of insv23B
Nl1N-ts1 is a suppressor | partially of trichogen cell phenotype of insv23B
Nl1N-ts1/N[+] is a suppressor of leg phenotype of Scer\GAL4bab1-GAL4-U, talUAS.cGa
Nl1N-ts1 is a suppressor of eye phenotype of upd1GMR.PB
Nl1N-ts1 is a suppressor of neuroblast | supernumerary & larval brain phenotype of aurA8839
Nl1N-ts1 is a suppressor | partially of basal cylinder phenotype of DlFE32
Nl1N-ts1 is a suppressor of tarsal segment 4 phenotype of DlFE32
Nl1N-ts1 is a suppressor of tarsal segment 3 phenotype of DlFE32
Nl1N-ts1 is a suppressor of eye phenotype of EgfrE3/EgfrE1
Nl1N-ts1 is a suppressor of phenotype of wgsev.PC
Nl1N-ts1 is a suppressor of phenotype of numb1
Other
Statement
Reference
Egfrtsla, Nl1N-ts1 has eye disc | heat sensitive phenotype
Nl1N-ts1, toc[-] has ovary phenotype
Additional Comments
Genetic Interactions
Statement
Reference
Expression of dysfScer\UAS.cJa under the control of Scer\GAL4ptc.PU in a Nl1N-ts1 mutant background (shifted to the permissive temperature at the third instar larval stage) results in a uniform and continuous tarsal cuticle with no joints and a fold running along the proximo-distal axis. In the corresponding leg discs a fold is seen along the proximo-distal axis.
CRMPunspecified enhances the penetrance of the pIIa-to-pIIb cell fate transformation seen in Nl1N-ts1 pupae placed at a semi-permissive temperature at the time of division of pI (sensory organ precursor) cells from 7.3% to 17.7%.
The ectopic microchaetae seen on the notum in Nl1N-ts1 females raised at 22[o]C are suppressed by insv23B. The pupal lethality caused by Nl1N-ts1 at 25[o]C is suppressed by homozygosity for insvunspecified. The double-socketed sensory organs on the abdomen which are seen in insv23B adults are largely suppressed by Nl1N-ts1 at 25[o]C.
Expression of DlΔIC.Scer\UAS under the control of Scer\GAL415J2 enhances the Nl1N-ts1 early axon phenotype. The Nl1N-ts1 pioneer axon phenotype is strongly enhanced by heterozygosity for fra2. The Nl1N-ts1 pioneer axon phenotype is strongly enhanced by heterozygosity for fra4. The Nl1N-ts1, Df(1)NetABΔ 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\GAL4repo-M1B suppresses the Nl1N-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\GAL415J2 fails to suppress the Nl1N-ts1 longitudinal pioneer axon phenotype. Abl4/+ suppresses the mature stage 16 CNS axonal phenotype of Nl1N-ts1. Expression of enaScer\UAS.T:Avic\GFP under the control of Scer\GAL415J2 suppresses the early longitudinal axon phenotype of Nl1N-ts1. Overexpression of cpbScer\UAS.cWa under the control of Scer\GAL415J2 enhances the early longitudinal axon phenotype of Nl1N-ts1. Overexpression of trioGEF1.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL415J2 enhances the early longitudinal axon phenotype of Nl1N-ts1. Overexpression of Rac1N17.Scer\UAS under the control of Scer\GAL415J2 suppresses the early longitudinal axon phenotype of Nl1N-ts1.
Inhibition of N activity through Nl1N-ts1 suppresses numbTS4D.Scer\UAS induced ectopic neuroblast formation.
The ectopic leg joint phenotype caused by expression of talScer\UAS.cGa under the control of Scer\GAL4bab1-GAL4-U is suppressed by Nl1N-ts1/+ (at the restrictive temperature).
Expressing dpnScer\UAS.cSa in clones under the control of Scer\GAL4Scer\FRT.Act5C suppresses neuroblast loss seen when Nl1N-ts1 is shifted to the restrictive temperature from the first instar larval stage onwards.
A trio123.4 heterozygous background significantly restores the ability of ISNb axons to enter the ventrolateral muscle field in Nl1N-ts1 mutants. This suppression is reverted upon pan-neural expression of trioScer\UAS.cBa under the control of Scer\GAL4elav-C155. Pan-neuronal expression of trioGEF1mu.Scer\UAS in a Nl1N-ts1; trio123.4/+ background (under the control of Scer\GAL4elav-C155) does not restore the ability of ISNb axons to enter the ventrolateral muscle field. Pan-neuronal expression of trioGEF2mu.Scer\UAS in a Nl1N-ts1; trio123.4/+ background (under the control of Scer\GAL4elav-C155) restores the ability of ISNb axons to enter the ventrolateral muscle field. Heterozygosity for Rac1J10 Rac2Δ MtlΔ suppresses the axonal defects found in Nl1N-ts1 mutants. Heterozygosity for Cdc424 or Rho1rev220 fails to suppress the axonal defects found in Nl1N-ts1 mutants. Expression of a constitutively active form of Rac1, Rac1V12.Scer\UAS under the control of Scer\GAL460, significantly increases the occurrence of ISNb bypass in Nl1N-ts1 embryos. Expression of Rac1N17.Scer\UAS under the control of Scer\GAL460, significantly increases the occurrence of ISNb bypass in Nl1N-ts1 embryos. The ISNb bypass phenotype of Nl1N-ts1 mutant embryos is not significantly modulated by expression of Rac1Scer\UAS.cLa under the control of Scer\GAL460. The ISNb bypass phenotype of Nl1N-ts1 mutant embryos is not significantly modulated by expression of Cdc42V12.Scer\UAS (under the control of Scer\GAL460) or Cdc42N17.Scer\UAS (under the control of Scer\GAL4elav-C155). The ISNb bypass phenotype of Nl1N-ts1 mutant embryos is not significantly modulated by expression of Rho1V14.Scer\UAS (under the control of Scer\GAL460) or Rho1N19.Scer\UAS (under the control of Scer\GAL4elav-C155).
Homozygous seqA41 clones in the thorax generated in Nl1N-ts1 animals grown at the restrictive temperature generate socket cells within the clone.
The retinal disorganisation and interommatidial pigment cell death observed in Chc4 mutant flies is suppressed in animals carrying a mutation in Nl1N-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 Dip3C00008 under the control of Scer\GAL4GMR.PF is partially suppressed by Nl1N-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 Nl1N-ts1 is inactivated in a l(2)gd124 mutant eye clones
Nl1N-ts1; ft8/ft422 double mutant larvae grown at restrictive temperature exhibit distal wing growth.
Extra R8 and other neurons differentiate and no second mitotic wave occurs in Nl1N-ts1, Egfrtsla 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.
The weak excess cardioblast phenotype seen in Nl1N-ts1 embryos raised at 30oC is dominantly enhanced by lqfARI.
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.
Most bristles are lost within phyl2 clones induced in Nl1N-ts1 flies in which N activity has been eliminated during 6-12 hours after puparium formation. Nl1N-ts1 ; phyl1/phyl2 embryos show a reduction in the number of neurons in each abdominal hemisegment.
Homozygous emc1 clones induced in a Nl1N-ts1/+ background result in thickening of the wing veins when pupal development takes place at 29oC (the restrictive temperature for the Nl1N-ts1 allele).
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.
Ca-P60A alleles cause dominant eye roughening and maldeposition of lens material between adjacent lenses, typical of the 'facet' mutant phenotype, in a Nl1N-ts1/Nfa-g62 background at 23oC.
In a numb796; Nl1N-ts1 double mutant the sib cell is usually transformed into an RP2 neuron, as in Nl1N-ts1 alone. However, this phenotype is only partially penetrant, as some hemisegments are seen with the numb transformation(RP2 to sib).
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.
The frequency of compound egg chambers in these females is reduced if the female is also heterozygous for ctC145 or ctdb10.
Nl1N-ts1 shi1 clones also exhibit a strong neurogenic phenotype, 7% bristles along the clone border are wild type. Occasionally adjacent wild type and mutant bristles are seen.
Removal of N activity can suppress the P{sev-wg.C} phenotype, almost complete loss of interommatidial bristles.
Double heterozygotes of Nl1N-ts1 with da2 show ovarian defects as for mutant da genotypes: stalkless ovaries, compound egg chambers and no distinction between germarium and vitellarium. Females doubly heterozygous for Nl1N-ts1 and Dl9 show compound egg chambers and missing stalks.
Xenogenetic Interactions
Statement
Reference
Expression of Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL415J2 enhances the early longitudinal axon phenotype of Nl1N-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.
Complementation and Rescue Data
Partially rescued by
Comments
Expression of NScer\UAS.cUa under the control of Scer\GAL4repo-M1B efficiently rescues the early axon phenotype of Nl1N-ts1 and restores restores the continuity of the neuronal meshwork. Expression of NScer\UAS.cUa under the control of Scer\GAL4htl.PM efficiently rescues the early axon phenotype of Nl1N-ts1. Expression of NScer\UAS.cUa under the control of Scer\GAL415J2 efficiently rescues the early axon phenotype of Nl1N-ts1. Expression of NFLNΔ10-12.Scer\UAS under the control of Scer\GAL415J2 fails to rescue the Nl1N-ts1 axon phenotype. Expression of N1893-2155.Scer\UAS in pioneer neurons under the control of Scer\GAL415J2 partially rescues axon extension in Nl1N-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.
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Shellenbarger.
Comments
Comments
The function of N during development of the adult sensilla has been studied using the temperature-sensitive allele Nl1N-ts1.
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.
Phenotypes of sno71e3 are similar to those of Nl1N-ts1.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (15)
Reported As
Symbol Synonym
Nl1-Nts1
Nts1
(Rice et al., 2015, Small et al., 2014, Peng et al., 2012, Hwang and Rulifson, 2011, Kuzina et al., 2011, Okegbe and DiNardo, 2011, Rebeiz et al., 2011, Seugnet et al., 2011, Song and Giniger, 2011, Ngo et al., 2010, Bernard et al., 2009, Peralta et al., 2009, Eun et al., 2008, Edenfeld et al., 2007, Song et al., 2007, Bernard et al., 2006, Micchelli and Perrimon, 2006, Ward et al., 2006, Apitz et al., 2005, Dobens et al., 2005, Grzeschik and Knust, 2005, Zhang et al., 2005, Aigouy et al., 2004, del Alamo Rodriguez et al., 2004, Dutta et al., 2004, Mandal et al., 2004, Merdes et al., 2004, Moore et al., 2004, Crowner et al., 2003, Kenyon et al., 2003, Lebestky et al., 2003, Rawls and Wolff, 2003, Barolo et al., 2002, Chou and Chien, 2002, Duvic et al., 2002, Pickup et al., 2002, Tang and Sun, 2002, Tsuda et al., 2002, Ben-Yaacov et al., 2001, Furriols and Bray, 2001, Mishra et al., 2001, Presente et al., 2001, Ramain et al., 2001, Udolph et al., 2001, van de Bor and Giangrande, 2001, Barolo et al., 2000, Flores et al., 2000, Gorski et al., 2000, Wesley and Saez, 2000, Zhao et al., 2000, Bishop et al., 1999, Fanto and Mlodzik, 1999, Haag et al., 1999, Ikeya and Hayashi, 1999, Larkin et al., 1999, Lesokhin et al., 1999, Ligoxygakis et al., 1999, Llimargas, 1999, Micchelli and Blair, 1999, Periz and Fortini, 1999, Rangarajan et al., 1999, Steneberg et al., 1999, Tomlinson and Struhl, 1999, Wai et al., 1999, Ye and Fortini, 1999, Ye et al., 1999, zur Lage and Jarman, 1999, Anant et al., 1998, Baker and Yu, 1998, Buescher et al., 1998, Fuerstenberg and Giniger, 1998, Giniger, 1998, Gonzalez-Reyes and St. Johnston, 1998, Martinez Arias, 1998, Sun et al., 1998, Baker and Yu, 1997, Grammont et al., 1997, Jackson and Blochlinger, 1997, Menne et al., 1997, Micchelli et al., 1997, Reddy et al., 1997, Seugnet et al., 1997, Baker et al., 1996, Cadigan and Nusse, 1996, de Celis et al., 1996, Dokucu et al., 1996, Goode et al., 1996, Hartenstein et al., 1996, Heitzler et al., 1996, Lee et al., 1996, Schweisguth et al., 1996, Baker and Zitron, 1995, Diaz-Benjumea and Cohen, 1995, Jennings et al., 1995, Rulifson and Blair, 1995, Zaffran et al., 1995, Clark et al., 1994, Couso and Martinez Arias, 1994, Cummings and Cronmiller, 1994, Fortini and Artavanis-Tsakonas, 1994, Li et al., 1994, Menne and Klambt, 1994, Muskavitch, 1994, Bodmer et al., 1993, Coyle-Thompson and Banerjee, 1993, Dickson and Hafen, 1993, Green et al., 1993, Heitzler and Simpson, 1993, Skaer, 1993, Hartenstein et al., 1992, Woods and Bryant, 1992, Xu et al., 1992, Heitzler and Simpson, 1991, Ruohola et al., 1991, Baker et al., 1990, Hartenstein and Posakony, 1990, Cagan and Ready, 1989, Dietrich and Campos-Ortega, 1984, Lehmann et al., 1983)
Name Synonyms
Secondary FlyBase IDs
    References (208)