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.
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.
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.
mutant clones in the eye imaginal disc are overgrown compared to controls.
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.
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.
mutant cell clones display a large size and occupy large territories of wing and eye discs.
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.
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
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.
heterozygotes do not exhibit an obvious dendritic phenotype.
The mid-pupal retina of wtsx1
animals contains a large excess of inter-ommatidial cells. The resulting adult eyes are distorted and lumpy.
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.
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.