Deletion of 400bp in the second intron. Generated by imprecise excision of P{PZ}ds05142.
abnormal cell polarity | somatic clone (with dsUAO71)
majority die during P-stage (with ds38k), with Scer\GAL4hh.PU, dsUAS.cTa
visible | adult stage (with dsUAO71)
The orientation of cell division is randomized in ds36D/dsUAO71 mitotic clones in wing discs. Therefore, in contrast to wild-type postmitotic cells, ds36D/dsUAO71 postmitotic cells do not show any preferential orientation. Mitotic recombination clones in ds36D/dsUAO71 mutant wings show a rounded shape, instead of the elongated shape seen in wild-type clones. At the adult stage, ds36D/dsUAO71 wings are shorter, rounder and wider than wild type. Likewise, ds36D/dsUAO71 mitotic clones in eye discs show a defective shape and preferential orientations of cell divisions are lost. Resulting adult eyes are rounder than wild type. ds36D/dsUAO71 flies also have shorter, wider legs than wild-type flies.
dsD36 has hyperplasia phenotype, enhanceable by MycUAS.cZa/Scer\GAL4hh.PU
MycUAS.cZa, Scer\GAL4hh.PU, dsD36 has increased cell size phenotype
dmScer\UAS.cZa overexpression clones (under the control of Scer\GAL4hh.PU) found in the posterior of the wing disc strongly enhance the proliferative activity of ds36D mutant cells. In addition these cells are larger in dmScer\UAS.cZa clones than in a wild-type background.
Instead of rescuing the wing defects of ds38k/ds36D transheterozygotes, the Scer\GAL4hh.PU-driven expression of either dsScer\UAS.cTa or dsintra.Scer\UAS.T:SV5\V5 leads to high lethality during early pupal stages and even enhances the wing defects in surviving adults.
The expression of dsex.Scer\UAS.T:Avic\GFP driven by Scer\GAL4hh.PU does not rescue the wing defects observed in ds38k/ds36D transheterozygotes.