UASt regulatory sequences drive expression of an inverted repeat.
The expression of Ptp52FGD2599 under the control of Scer\GAL4Myo31DF-NP0001 leads to the following defects in the larval midgut, as compared to controls: decreased numbers of autophagosomes, identified as fluorescent Atg8a puncta, and autolysosomes, identified as fluorescent Lysotracker puncta, in the gastric caecum cells during third instar larval stage; decrease in the levels of apoptosis in the gastric caecum cells during puparium formation; delayed histolysis of larval midgut and delayed removal of the gastric caeca during metamorphosis in a significant proportion of individuals. Similar delays in histolysis of larval midgut and in the removal of the gastric caeca during metamorphosis are also observed upon expression under the combined control of Scer\GAL4tub.PU and Gal80[ts], induced only from the second instar larval stage onwards, as compared to controls.
Adults expressing Ptp52FGD2599 under the control of Scer\GAL4elav.PLu (in the presence of Dcr-2Scer\UAS.cDa to increase the efficiency of RNAi) do not show a significant defect in avoidance of noxious temperature (46[o]C) compared to control flies.
Expression under the control of Scer\GAL4Mef2.PR results in adult/pharate lethality.