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General Information
Symbol
Dmel\wtsx1
Species
D. melanogaster
Name
FlyBase ID
FBal0044527
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
latsX1, wtslatsX1
Mutagen
    Nature of the Allele
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference
    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 ( 1 )
    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
    dorsal multidendritic neuron ddaC | somatic clone & dendritic tree
    Detailed Description
    Statement
    Reference
    wtsx1 homozygous clones in the third instar larval wing disc are larger than control clones.
    Somatic clones of wtsx1 homozygous cells in the wing disc overgrow and are larger than their control twinspot clones in the third instar larval wing disc.
    wtsx1/wtsx1 somatic clones of type I lineages in the ventral nerve cord of third instar larvae in a heterozygous background have significantly smaller neurons, but an overall increased clone volume compared to controls.
    wtsx1 homozygous mutant embryos from mothers whose germline consisted entirely of wtsx1 mutant cells (generated by the Ovo[D] germline clone method), and which thus are both zygotically and maternally wtsx1 mutant, display a significant increase in the frequency of hemisegments with abnormal number of neurons in the asymmetrically dividing RP2 neural lineage. No such significant increase is observed in only zygotically mutant embryos although they do display defective asymmetric division of heart and muscle progenitors P2 and P15 resulting in high proportion of hemisegments with either duplications or losses of muscle and pericardial cells. Embryos both zygotically and maternally mutant for wtsx1 display defects in the asymmetric neuroblast (NB) division: disturbed asymmetric localization of polarity and cell-fate determinants, high frequency of mitotic spindle orientation defects as well as frequent failure to produce two NB daughter cells of the characteristic unequal size. The type II brain neuroblast somatic clones homozygous mutant for wtsx1 display defects in asymmetric cell division: mislocalization of asymmetrically distributed proteins as well as mitotic spindle orientation defects.
    wtsx1 mutant clones in the eye imaginal disc are overgrown compared to controls.
    wtsx1 mutant wings disc clones are overgrown.
    Approximately 60% of wtsx1 mutant border cell clusters are delayed at stage 10 of oogenesis. Unlike control clusters, F-actin fails to polarize to the outer rim of wtsx1 mutant clusters and instead tends to accumulate throughout the cluster. Border cell specification is not affected in these mutants.
    Cells in homozygous clones in the wing disc accumulate F-actin near the apical surface.
    Homozygous clones in the eye show progressive degeneration of photoreceptor cells.
    wtsx1 mutants show a progressive loss of dendritic branches in class IV neurons without affecting axons.
    Clones of tissue harbouring wtsx1 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 wtsx1 clones are generated using eyFlp/MARCM, with wtsx1 clones occupying almost the entire eye disc. Very few presumptive ommatidial clusters are observed and there is no obvious sign of the morphogenetic furrow.
    wtsx1 mutant cell clones display a large size and occupy large territories of wing and eye discs.
    wtsx1 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 wtsx1 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.
    wtsx1 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, wtsx1 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, wtsx1 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. wtsx1 heterozygotes do not exhibit an obvious dendritic phenotype.
    The mid-pupal retina of wtsx1/wtsx1 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.
    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    NOT Enhanced by
    Statement
    Reference
    wtsx1 has neuroanatomy defective phenotype, non-enhanceable by sav3
    Suppressed by
    Statement
    Reference
    wtsx1 has tumorigenic phenotype, suppressible by Hsap\LATS1hs.PT
    NOT suppressed by
    Enhancer of
    Statement
    Reference
    wtsx1/wts[+] is an enhancer of visible | dominant phenotype of Pc3
    wtsx1/wts[+] is an enhancer of visible | dominant phenotype of Pc1
    wtsx1/wts[+] is an enhancer of hyperplasia | recessive phenotype of exAP49
    NOT Enhancer of
    Statement
    Reference
    wtsx1/wts[+] is a non-enhancer of visible | adult stage phenotype of MagiUAS.GFP, Scer\GAL4GMR.PU
    wtsx1/wts[+] is a non-enhancer of neuroanatomy defective phenotype of hpoMGH4
    wtsx1 is a non-enhancer of tumorigenic | somatic clone phenotype of matse235
    Suppressor of
    NOT Suppressor of
    Other
    Statement
    Reference
    Fancd2dsRNA.UAS, Scer\GAL4ey.PU, wtsx1/wts[+] has visible | chemical conditional phenotype
    Mnn1e200, Scer\GAL4ey.PU, wtsx1/wts[+] has visible | chemical conditional phenotype
    Mnn1e200, Scer\GAL4ey.PU, wtsx1/wts[+] has tumorigenic | conditional phenotype
    Phenotype Manifest In
    NOT Enhanced by
    Statement
    Reference
    wtsx1 has dorsal multidendritic neuron ddaC | somatic clone & dendritic tree phenotype, non-enhanceable by sav3
    Suppressed by
    NOT suppressed by
    Statement
    Reference
    Enhancer of
    Statement
    Reference
    wtsx1/wts[+] is an enhancer of wing phenotype of Fbxl7JF01515, Scer\GAL4nub-AC-62
    wtsx1/wts[+] is an enhancer of mesothoracic leg phenotype of Pc1
    wtsx1/wts[+] is an enhancer of metathoracic leg phenotype of Pc1
    wtsx1/wts[+] is an enhancer of sex comb | ectopic phenotype of Pc3
    wtsx1/wts[+] is an enhancer of mesothoracic leg phenotype of Pc3
    wtsx1/wts[+] is an enhancer of metathoracic leg phenotype of Pc3
    wtsx1/wts[+] is an enhancer of sex comb | ectopic phenotype of Pc1
    wtsx1/wts[+] is an enhancer of wing disc phenotype of exAP49
    NOT Enhancer of
    Statement
    Reference
    wtsx1/wts[+] is a non-enhancer of eye | adult stage phenotype of MagiUAS.GFP, Scer\GAL4GMR.PU
    wtsx1/wts[+] is a non-enhancer of multidendritic dendrite phenotype of hpoMGH4
    Suppressor of
    NOT Suppressor of
    Other
    Statement
    Reference
    Fancd2dsRNA.UAS, Scer\GAL4ey.PU, wtsx1/wts[+] has eye | chemical conditional phenotype
    Mnn1e200, Scer\GAL4ey.PU, wtsx1/wts[+] has eye | chemical conditional phenotype
    Pc3, wtsx1/wts[+] has dendrite & dorsal multidendritic neuron ddaC | somatic clone phenotype
    sav3, wtsx1/wts[+] has dorsal multidendritic neuron ddaC | somatic clone & dendritic tree phenotype
    Additional Comments
    Genetic Interactions
    Statement
    Reference
    Clones that are both wtsx1 homozygous and express sdKK108877 under the control of Scer\GAL4Tub.PU are lethal in the wing.
    The size (normalized to the respective twinspots) of wtsx1;Chchd3D1 double mutant somatic clones in the wing disc is intermediate between the overgrowing wtsx1 clones and under-growing Chchd3D1 clones but larger than the control wild-type clones.
    wtsx1/wtsx1 somatic clones in a heterozygous background expressing ykiKK109756 under the control of Scer\GAL4Tub.PU display an overall decrease in type I lineage clone volume in the ventral nerve cord of third instar larvae compared to controls.
    The increased number of satellite boutons on neuromuscular junctions in third instar larvae expressing StripdsRNA.shRNA.Scer\UAS.9 under the control of Scer\GAL4RapGAP1-OK6 is suppressed by combination with a single copy of wtsx1.
    The proportion of hemisegments with abnormal number of neurons in the asymmetrically dividing RP2 neural lineage is significantly increased in embryos that are double heterozygous for wtsx1 and any of the following: cno2, Rap1P5709, aPKCk06403, baz4, inscP49, pinsΔ50, GαiKG01907, Khc-73MI02026, scrib1, pros17, numb1 or aurA87Ac-3. No such significant increase is observed in embryos double heterozygous for wtsx1 and either mud4 or l(2)gl4.
    The rough eye phenotype observed in adults expressing MagiScer\UAS.T:Avic\GFP under the control of Scer\GAL4GMR.PU is not modified by combination with single copy of wtsx1.
    Expression of hppyScer\UAS.cZa under the control of Scer\GAL4tub.PU does not suppress growth in wtsx1 mutant wing disc clones.
    The increased size of wtsx1 clones is not rescued by Fbxl7Scer\UAS.T:Zzzz\FLAG expression.
    wtsx1 rescues the reduction in eye disc clone size seen when par-1HMS00405 is expressed under the control of Scer\GAL4unspecified, with the resulting clones similar in size to those seen with wtsx1 alone.
    Expression of TgiScer\UAS.B suppresses the overgrowth seen in wtsx1 mutant wing disc clones, resulting in a reduced clone size compared to wild type, similar to the phenotype seen in clones expressing TgiScer\UAS.B alone.
    Overexpression of cpbScer\UAS.cWa is able to fully suppress the migration defect and F-actin polarisation defects of wtsx1 mutant border cell clusters.
    Whereas wtsx1 ddaC MARCM clones show a simplifed dendritic arbor with significantly reduced numbers of terminal branches, wtsx1 clones overexpressing NmnatScer\UAS.cZa under the control of Scer\GAL4elav-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 NmnatΔ4790-2 and wtsx1 does not show any synthetic phenotypes in affecting axon or dendrite development of class IV neurons.
    When Wbp2KK108304 or Wbp2GD7170 is expressed in wtsx1-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 Wbp2KK108304 or Wbp2GD7170 is expressed in wtsx1-deficient tissues using eyFlp/MARCM, eye disc size is reduced, the amount of wtsx1 tissue relative to wild type tissue is decreased, and the differentiation of the developing eye is almost completely restored.
    Expression of exScer\UAS.P\T.T:Avic\GFP-EGFP under the control of Scer\GAL4tub.PU largely suppresses the overgrowth phenotype seen in wtsx1 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 exCT.Scer\UAS.P\T.T:Avic\GFP-EGFP under the control of Scer\GAL4tub.PU partially suppresses the pupal stage lethality seen following the induction of wtsx1 larval eye disc clones. Expression of exlinker.Scer\UAS.P\T.T:Avic\GFP-EGFP under the control of Scer\GAL4tub.PU is unable to suppress the overgrowth phenotype seen in wtsx1 larval eye disc clones. The pupal stage lethality is also not rescued.
    The growth advantage of wtsx1 clones in the wing disc over their wild-type twin spots is not affected if the clones are also homozygous for crb2.
    Expression of Fancd2dsRNA.Scer\UAS in the eyes under the control of Scer\GAL4ey.PU enhances the rate of eye tumor formation in wtsx1/+ mutant flies treated with nitrogen mustard. A Mnn1e200 mutant background enhances the rate of eye tumor formation in response to nitrogen mustard compared to wtsx1/+ mutant controls.
    The eye overgrowth phenotype caused by wtsx1 clones is almost completely suppressed by co-expression of sddsRNA.N.Scer\UAS and sddsRNA.C.Scer\UAS under the control of Scer\GAL4tub.
    Pc3/wtsx1 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 Pc3/+ males is enhanced by wtsx1. The ectopic sex comb phenotype seen on the second and third legs of Pc1/+ males is enhanced by wtsx1/+.
    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 wtsx1 mutant background allows recovery of larval wing disc clones expressing exScer\UAS.cBa under the control of Scer\GAL4Scer\FRT.Act5C.
    The p53GMR.Ex-mediated induction of apoptosis in the posterior portion of late larval eye discs is reduced in wtsx1 clones.
    sav3/wtsx1 transheterozygotes exhibit simplified dendrites similar to moderately affected sav3 MARCM clones. These double mutants show a severe dendrite effect comparable to wtsx1 MARCM clones. Transheterozygotes for wtsx1/hpoMGH4 display simplified dendrites similar to wtsx1 mutants. Transheterozygotes for wtsx1/trc1 do not show any significant dendritic phenotypes.
    Wing disc overgrowth seen in exAP49 homozygous late third instar larvae is enhanced by wtsx1/+.
    The loss of inter-ommatidial cells in the developing retinas of exScer\UAS.cBa; Scer\GAL4GMR.PF animals at the mid-pupal stage is completely suppressed in wtsx1/wtsx1 somatic clones. The resulting clones have an excess of inter-ommatidial cells as do wtsx1/wtsx1 somatic clones do. Heterozygosity for wtsx1 partially suppresses the reduction in size and patterning defects seen in the eyes of exScer\UAS.cBa; Scer\GAL4GMR.PF animals. The adult eye phenotype and the loss of interommmatidial cells seen in hpoScer\UAS.cUa; Scer\GAL4GMR.PF mid-pupal retinas is suppressed by wtsx1/wtsx1.
    Overexpression of Akt1Scer\UAS.T:Ivir\HA1 (under the control of Scer\GAL4Act5C.PI) using the FLP/FRT system in brain somatic clones mutant for scrib1 and wtsx1 does not cause metastatic behaviour despite accelerated tumour growth.
    Expression of Fancd2dsRNA.Scer\UAS in the eyes under the control of Scer\GAL4ey.PU in a wtsx1/+ 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 ftΔECD.Scer\UAS phenotype (under the control of Scer\GAL4nub-AC-62) is suppressed by wtsx1 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.
    The Scer\GAL4C5-driven hpoScer\UAS.cUa cell death phenotype observed in the wing can be partially suppressed through wtsx1 heterozygosity.
    Xenogenetic Interactions
    Statement
    Reference
    A significantly enhanced rate of loss of heterozygosity in wtsx1 heterozygotes is only seen when both Hsap\AS3MTScer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4da.G32 and the flies are exposed to inorganic arsenicals.
    Expression of Hsap\LATS1 using heat shock in flies containing wtsx1 clones suppresses tumour formation, and the wtsx1 cells develop into normal adult structures.
    Complementation and Rescue Data
    Fails to complement
    Comments
    Images (0)
    Mutant
    Wild-type
    Stocks (1)
    Notes on Origin
    Discoverer
    Comments
    Comments
    Strong wts allele.
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (13)
    Reported As
    Symbol Synonym
    wartslatsX1
    Name Synonyms
    Secondary FlyBase IDs
      References (75)