The reduced size of regenerated adult wings characteristic for mole02670 heterozygous mutants that were subjected to ablation of the imaginal wing disc tissue during the larval stage can be rescued by combination with a single copy of pucE69.
Reduced resistance to oxidative stress (paraquat) in Mrp4M2/Mrp4M2 flies is increased to significantly more than wild type levels with a single copy of pucE69. Reduced lifespan in Mrp4M1/Mrp4M2 flies is increased to significantly more than wild type levels with a single copy of pucE69. Reduced climbing ability in Mrp4M1/Mrp4M2 flies is rescued to wild type levels (at 10 and 30 days old) and increased beyond wild type levels (at 40 days old) by a single copy of pucE69.
Introduction of a single copy of pucE69 into the Scer\GAL4GMR.PF, egrScer\UAS.cIa background dramatically enhances the reduced eye phenotype, with flies displaying a prominent black lesion in place of the eye.
The ectopic apoptosis seen in the wing discs of pucE69/+ Cskj1D8/+ double heterozygotes is enhanced if they are also heterozygous for ASPP8, resulting in adults with a severely reduced wing size. These adults also have leg deformities.
Only 20% of embryos derived from DokPG155 germ-line clones that are also heterozygous for pucE69 show a dorsal closure phenotype, compared to 48% of DokPG155 germ-line clones without a puc mutation. The rescued embryos have small holes in the cuticle.
pucE69/+ strongly enhances the loss of apical profile, delamination and subsequent migration and cell death increase seen in cells at the posterior edge of theptc expression domain in CskIR.Scer\UAS Scer\GAL4ptc-559.1 third instar larvae.
The reduced survival rate after natural infection with "Ecc-15" (P.carotovorum.carotovorum) that is seen in flies expressing IrcdsRNA.Scer\UAS under the control of Scer\GAL4da.G32 is partially rescued by pucE69/+.
Recovery of arr2 homozygous somatic clones in third instar wing discs (induced at around 60 hours after egg laying) is reduced by the presence of pucE69/+ (10/25 twinspots vs 21/29 in a wild-type background).
pucE69/+; hep1/Y mutant flies have a decreased mortality rate in response to paraquat compared to hep1/Y single mutants, but an increased mortality rate compared to pucE69/+ single mutants. Likewise, pucE69/+; bsk2/+ have a decreased sensitivity to paraquat compared to bsk2/+ single mutants and an increased mortality rate compared to pucE69/+ single mutants. The response of pucE69/+ flies to paraquat is not affected when flies have a ry506 genetic background. pucE69/+ flies with a hep1/Y background have a less pronounced extension of lifespan than pucE69/+ single mutant flies.
pucE69 Sac1L2F double heterozygous embryos show defects in the dorsal cuticle (anterior head holes and/or puckering). pucE69 shows no genetic interactions with Sac12107 or Sac1BG02228. Sac1L16C interacts genetically with pucE69.
The dorsal closure phenotype caused by expression of egScer\UAS.cDa under the control of Scer\GAL4pnr-MD237 is suppressed by pucE69. The dorsal closure phenotype caused by expression of knrlScer\UAS.cLa under the control of Scer\GAL4pnr-MD237 is suppressed by pucE69.
The severe dorsal open phenotype of slpr921/Y embryos is significantly rescued by pucE69/+. pucE69/+ rescues slpr3P5/Y animals to adulthood. The mutant male flies are weakly viable with no gross morphological defects.
Dominantly suppresses the lethality and cleft thorax phenotypes of Src42AJp45 homozygotes.
Homozygous escapers show mildly roughened eyes that display typical planar polarity defects.
Dominantly enhances the wing notching phenotype of dppd8/dpphr56, tkv7/tkv427 or biomb-1/Y flies. Dominantly enhances the appearance of an apoptotic cluster of cells in the primordial wing tip of the late third larval instar tkv7/tkv427 wing disc. The appearance of the cluster of apoptotic cells is suppressed in hepr75/Y ; tkv7/tkv427; pucE69/+ larvae.
The lethality of the kay1/kay2 combination is rescued by one copy of pucE69; the rescued flies have a thoracic cleft phenotype ranging from strong to very mild. Rescues the thoracic cleft phenotype of kay2 homozygotes. The lethality of embryos which are maternally and zygotically hep1 is rescued by one copy of pucE69. The lethality of pucE69 homozygotes is rescued if the flies are also homozygous or hemizygous for hep1. The rescued flies look remarkably normal, except some females have macrochaetae with a kink. Dominantly enhances the scutellar phenotype caused by hepScer\UAS.cBa expressed under the control of Scer\GAL4pnr-MD237.