G to A nucleotide change at the splice acceptor of the first intron in the coding region. The resulting transcript has a single base deletion of a G at the beginning of exon 2 and encodes only the first 21 amino acids of rok followed by a 35 amino acid random peptide and a stop codon.
filamentous actin & nurse cell | germ-line clone
filamentous actin & oocyte | germ-line clone
mushroom body & axon | somatic clone
plasma membrane & oocyte | germ-line clone
rok2 clones generated in PtenJF01859-expressing tissue suppresses the effect of the expression of PtenJF01859 under the control of Scer\GAL80ts.αTub84B and Scer\GAL4en.PU on cell packing, namely the excess of short junctions. Despite a slightly higher proportion of non-rearranging junctions (1.15-fold), the rearranging junctions neither produce an excess of short junctions nor fluctuate extensively, but lengthen to produce long cell junctions as observed in wild-type tissue. Furthermore, the packing and cell rearrangement dynamics in the double mutant tissue is similar to the one observed in rok2 single mutant tissue.
The wing discs of Drakdel rok2/DrakKO third instar larvae are composed of unusually thin epithelial layers which are grossly distorted. The wing pouch region has folds which project basally out of the plane of the epithelium, and these distortions are accompanied by massive apoptosis.
100% of Drakdel rok2 double homozygous embryos die before hatching. They show a fully penetrant head defect, which is characterized by an anterior hole in the embryonic cuticle and anterior malformations of the cephalopharyngeal skeleton.
The multiple wing hair phenotype caused by expression of towScer\UAS.cCa under the control of Scer\GAL4hs.PB using heat shock at 24 hours after puparium formation is enhanced if the flies are also carrying one copy of rok2.
rok2 shows a strong interaction (at least 50% of double heterozygotes have at least one malformed leg) with the following mutations: Sb70. rok2 shows a moderate interaction (25-49% of double heterozygotes have at least one malformed leg) with the following mutations: Sb63b. rok2 shows a weak interaction (5-24% of double heterozygotes have at least one malformed leg) with the following mutations: Df(3R)sbd105 and Rho112-6. Sbsbd-201/Sbsbd-1 shows a weak interaction (5-24% of double mutants have at least one malformed leg) with the following mutations: rok2/+.
Addition of rok2 to dsh1 mutants results in a 2.5-fold increase in the number of multiple wing hair cells compared to dsh1 single mutants. 4% of rok2/Y ; sqhE20.E21/+ flies survive to adulthood. The multiple wing hair phenotype caused by rok2 is almost completely suppressed by sqhE20.E21.