|Feature type||allele||Associated gene||Dmel\wts|
|Also Known As||latsX1, wtslatsX1|
|Allele class||loss of function allele, amorphic allele - genetic evidence|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
dorsal multidendritic neuron ddaC | somatic clone & dendritic tree
Cells in homozygous clones in the wing disc accumulate F-actin near the apical surface.
wts[x1] mutants show a progressive loss of dendritic branches in class IV neurons without affecting axons.
Clones of tissue harbouring wts[x1] generated in the eye using the eyFlp/MARCM system overgrow dramatically and cause lethality at late third instar larval or early pupal stages of development. Eye discs substantially over-grow when wts[x1] clones are generated using eyFlp/MARCM, with wts[x1] clones occupying almost the entire eye disc. Very few presumptive ommatidial clusters are observed and there is no obvious sign of the morphogenetic furrow.
wts[x1] mutant cell clones display a large size and occupy large territories of wing and eye discs.
wts[x1] mutant MARCM clones contain 5-7 cells per clone, compared to 2-3 cells in wild-type clones. These clones contain differentiated absorptive enterocytes and secretory enteroendocrine cells indicating that intestine stem cell differentiation continues as in wild-type.
Induction of wts[x1] clones in third instar larval eye discs (generated using the eyFLP technique) results in massive overgrowth, with mutant cells covering almost the entire eye disc. The discs appear deformed with a folded excessive epithelium. No animals progress beyond the pupal stage.
Homozygous clones in the wing disc have a growth advantage; the ratio of mutant clone area: area of the wild-type twin spot is 2.93.
wts[x1] homozygous mutant clones generated in the male germline develop normally. 16 cells are observed per cyst, and cell size and morphology are indistinguishable from neighbouring control cells.
Adult eyes carrying homozygous mutant clones are overgrown.
Mutant eye discs (generated using the eyFLP-cell lethal system) show epithelial disorganisation. Neuronal differentiation is strongly impaired in these eye discs.
Heterozygous larvae show no significant defects in dendrite morphology of ddaC neurons. Heterozygous males do not have ectopic sex combs on the second or third legs.
Eye and wing imaginal discs heterozygous for wtsx1 are normal in size and morphology and are indistinguishable from wild-type discs.
Apoptosis is reduced by up to 3-fold in wtsx1 clones of wing or eye discs in response to γ-rays compared to wild-type tissue.
Compared to wild-type ddaC (dorsal dendrite arborization neuron C) neurons, wts[x1] MARCM clones exhibit a severe and highly penetrant simplification of dendritic trees, with a significantly reduced number and length of dendritic branches, and hence a greatly reduced dendritic field. In contrast to the severe dendritic defects caused by loss of wts function, wts[x1] MARCM clones of ddaC axons enter the ventral nerve cord at the appropriate position and show arborization patterns very similar to wild-type controls, with their axons terminating on the innermost fascicle and sending ipsilateral branches anteriorly and posteriorly and sometimes also a collateral branch towards the midline. wts[x1] heterozygotes do not exhibit an obvious dendritic phenotype.
The mid-pupal retina of wts[x1]/wts[x1] animals contains a large excess of inter-ommatidial cells. The resulting adult eyes are distorted and lumpy.
wtsx1 adults show tumor formation at extremely high penetrance. Each tumor represents a separate event as the tumors do not metastasize.
Mutant clones in the eye disc result in noninvasive tumours that never move from the head region.
When somatic clones of wtsx1 homozygous cells are generated throughout the eye disc using Scer\FLP1ey.PN, none resulting animals survive to eclosion.
When wtsx1 clones are made in the developing eye more cell divisions are seen than in wild-type cells. Also the normal cell death that occurs in the retina is almost completely abolished.
Lethal period is late embryonic and first larval instar. Mutant clones induced in first larval instar can be as large as 1/5 of the body size.
|NOT Enhanced by|
wtsx1 has lethal | somatic clone | pupal stage phenotype, suppressible | partially by exCT.Scer\UAS.P\T.T:Avic\GFP-EGFP/Scer\GAL4tub.PU
wtsx1 has lethal | somatic clone | pupal stage phenotype, suppressible | partially by exScer\UAS.P\T.T:Avic\GFP-EGFP/Scer\GAL4tub.PU
wtsx1 has size defective | somatic clone | third instar larval stage phenotype, suppressible | partially by exScer\UAS.P\T.T:Avic\GFP-EGFP/Scer\GAL4tub.PU
|NOT suppressed by|
wtsx1 has lethal | somatic clone | pupal stage phenotype, non-suppressible by Scer\GAL4tub.PU/exlinker.Scer\UAS.P\T.T:Avic\GFP-EGFP
|NOT Enhancer of|
wtsx1/wts[+] is a suppressor | partially of increased cell death phenotype of Scer\GAL4C5/Scer\GAL4C5, hpoScer\UAS.cUa
wtsx1/wtsx1 is a suppressor | partially of increased cell death | third instar larval stage phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, exScer\UAS.cBa
|NOT Suppressor of|
|Phenotype Manifest In|
|NOT Enhanced by|
wtsx1 has class IV dendritic arborizing neuron phenotype, suppressible by Scer\GAL4elav-C155/NmnatScer\UAS.cZa
wtsx1 has eye | somatic clone phenotype, suppressible by sddsRNA.C.Scer\UAS/Scer\GAL4tub.PU/sddsRNA.N.Scer\UAS
wtsx1 has eye disc | somatic clone phenotype, suppressible | partially by exScer\UAS.P\T.T:Avic\GFP-EGFP/Scer\GAL4tub.PU
wtsx1 has morphogenetic furrow | somatic clone phenotype, suppressible by Wbp2KK108304/Scer\GAL4αTub84B.PL
|NOT suppressed by|
wtsx1 has eye disc | somatic clone phenotype, non-suppressible by Scer\GAL4tub.PU/exlinker.Scer\UAS.P\T.T:Avic\GFP-EGFP
|NOT Enhancer of|
wtsx1/wts[+] is a suppressor | partially of wing phenotype of Scer\GAL4C5/Scer\GAL4C5, hpoScer\UAS.cUa
wtsx1/wtsx1 is a suppressor | partially of eye disc | third instar larval stage phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, exScer\UAS.cBa
wtsx1/wtsx1 is a suppressor of inter-ommatidial cell | pupal stage phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, exScer\UAS.cBa
wtsx1/wtsx1 is a suppressor of inter-ommatidial cell | pupal stage phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, hpoScer\UAS.cUa
Whereas wts[x1] ddaC MARCM clones show a simplifed dendritic arbor with significantly reduced numbers of terminal branches, wts[x1] clones overexpressing Nmnat[Scer\UAS.cZa] under the control of Scer\GAL4[elav-C155] elaborate dendrites with terminal branch numbers that do not differ statistically from wild-type controls. A similar rescue is seen in class IV neurons. A transheterozygous combination of Nmnat[Δ4790-2] and wts[x1] does not show any synthetic phenotypes in affecting axon or dendrite development of class IV neurons.
When Wbp2[KK108304] or Wbp2[GD7170] is expressed in wts[x1]-deficient tissues using eyFlp/MARCM, a significant increase in survival is observed with the majority of flies now reaching late pupal stages and forming pharate adults, with a small number emerging as fully developed adults. When Wbp2[KK108304] or Wbp2[GD7170] is expressed in wts[x1]-deficient tissues using eyFlp/MARCM, eye disc size is reduced, the amount of wts[x1] tissue relative to wild type tissue is decreased, and the differentiation of the developing eye is almost completely restored.
Expression of ex[Scer\UAS.P\T.T:Avic\GFP-EGFP] under the control of Scer\GAL4[tub.PU] largely suppresses the overgrowth phenotype seen in wts[x1] larval eye disc clones. The eye discs are no longer drastically deformed and retain a more normal shape. The pupal stage lethality is also partially rescued. Expression of ex[CT.Scer\UAS.P\T.T:Avic\GFP-EGFP] under the control of Scer\GAL4[tub.PU] partially suppresses the pupal stage lethality seen following the induction of wts[x1] larval eye disc clones. Expression of ex[linker.Scer\UAS.P\T.T:Avic\GFP-EGFP] under the control of Scer\GAL4[tub.PU] is unable to suppress the overgrowth phenotype seen in wts[x1] larval eye disc clones. The pupal stage lethality is also not rescued.
The growth advantage of wts[x1] clones in the wing disc over their wild-type twin spots is not affected if the clones are also homozygous for crb.
Expression of Fancd2[dsRNA.Scer\UAS] in the eyes under the control of Scer\GAL4[ey.PU] enhances the rate of eye tumor formation in wts[x1]/+ mutant flies treated with nitrogen mustard. A Mnn1[e200] mutant background enhances the rate of eye tumor formation in response to nitrogen mustard compared to wts[x1]/+ mutant controls.
The eye overgrowth phenotype caused by wts[x1] clones is almost completely suppressed by co-expression of sd[dsRNA.N.Scer\UAS] and sd[dsRNA.C.Scer\UAS] under the control of Scer\GAL4[tub].
Pc/wts[x1] double heterozygous larvae show dendritic defects in ddaC neurons; there is a significant reduction in the number of dendritic branchpoints. The ectopic sex comb phenotype seen on the second and third legs of Pc/+ males is enhanced by wts[x1]. The ectopic sex comb phenotype seen on the second and third legs of Pc/+ males is enhanced by wts[x1]/+.
ft8/ft422 mutants, heterozygous for wtsx1 exhibit a significant increase in size, both from wild-type and the ft8/ft422 double mutant, and display an even more 'rippled' morphology.
A wts[x1] mutant background allows recovery of larval wing disc clones expressing ex[Scer\UAS.cBa] under the control of Scer\GAL4[Scer\FRT.Act5C].
The p53GMR.Ex-mediated induction of apoptosis in the posterior portion of late larval eye discs is reduced in wtsx1 clones.
sav/wts[x1] transheterozygotes exhibit simplified dendrites similar to moderately affected sav MARCM clones. These double mutants show a severe dendrite effect comparable to wts[x1] MARCM clones. Transheterozygotes for wts[x1]/hpo[MGH4] display simplified dendrites similar to wts[x1] mutants. Transheterozygotes for wts[x1]/trc do not show any significant dendritic phenotypes.
The loss of inter-ommatidial cells in the developing retinas of ex[Scer\UAS.cBa]; Scer\GAL4[GMR.PF] animals at the mid-pupal stage is completely suppressed in wts[x1]/wts[x1] somatic clones. The resulting clones have an excess of inter-ommatidial cells as do wts[x1]/wts[x1] somatic clones do. Heterozygosity for wts[x1] partially suppresses the reduction in size and patterning defects seen in the eyes of ex[Scer\UAS.cBa]; Scer\GAL4[GMR.PF] animals. The adult eye phenotype and the loss of interommmatidial cells seen in hpo[Scer\UAS.cUa]; Scer\GAL4[GMR.PF] mid-pupal retinas is suppressed by wts[x1]/wts[x1].
Overexpression of Akt1[Scer\UAS.T:Ivir\HA1] (under the control of Scer\GAL4[Act5C.PI]) using the FLP/FRT system in brain somatic clones mutant for scrib and wts[x1] does not cause metastatic behaviour despite accelerated tumour growth.
Expression of Fancd2[dsRNA.Scer\UAS] in the eyes under the control of Scer\GAL4[ey.PU] in a wts[x1]/+ mutant background does not enhance the rate of eye tumor formation compared to controls in normal conditions. However the number of eye tumors is significantly increased when flies are treated with either nitrogen mustard or cisplatinum. This increase is restricted to eye tumors; the rate of tumours in other anatomical locations is similar to controls.
The ft[ΔECD.Scer\UAS] phenotype (under the control of Scer\GAL4[nub-AC-62]) is suppressed by wts[x1] heterozygosity.
mei-41unspecified; wtsx1/+ flies show a higher tumor incidence than controls, with a 2-fold increase at baseline and >10-fold increase after treatment with ionizing radiation. Homozygous Mnn1e200 mutants (Df(2L)Mnn1e200 mutants in which milt function is rescued by expression of the milt+22 transgene) that have a wtsx1/+ background show a two-fold greater number of tumorigenic foci than wtsx1/+ single mutants. After treatment with ionizing radiation, the number of tumorigenic foci is two to three times higher in these mutants than in controls and is 7-fold higher after treatment with nitrogen mustard.
scrib1 wtsx1 double mutant clones in the eye disc produce tumours which do not show metastatic behaviour. Expression of Akt1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4Act5C.PI in scrib1 wtsx1 double mutant clones in the eye disc increases tumour size but does not result in metastatic behaviour.
A significantly enhanced rate of loss of heterozygosity in wts[x1] heterozygotes is only seen when both Hsap\AS3MT[Scer\UAS.T:Ivir\HA1] is expressed under the control of Scer\GAL4[da.G32] and the flies are exposed to inorganic arsenicals.
|Complementation & Rescue Data|
|Fails to complement|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 12 )|
|Secondary FlyBase IDs|
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