UASt regulatory sequences drive expression of an inverted repeat.
The expression of AMPKαGD736, driven by Scer\GAL4NP0001 or driven by Scer\GAL4hs.PB and induced by 29[o]C, but not when driven by Scer\GAL4ppl.PU, induces significantly higher mortality to Ecc15 enteric infection, as compared to controls; Scer\GAL4NP0001-driven expression also abolishes the Ecc15 infection-induced lipid droplet autophagy (dual LS2- and Atg8-positive puncta) in the adult midgut observed in controls.
Adults expressing AMPKαGD736 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.
Depending on the insertion line used, expression under the control of Scer\GAL4Mef2.PR can result in early pupal lethality or undefined lethality.
AMPKαGD736, Scer\GAL4hs.PB has increased mortality | adult stage | conditional phenotype, suppressible by AccKK102082, Scer\GAL4hs.PB
AMPKαGD736, Scer\GAL4hs.PB has abnormal immune response | adult stage phenotype, suppressible by AccKK102082, Scer\GAL4hs.PB
AMPKαGD736, Scer\GAL4hs.PB has increased mortality | adult stage | conditional phenotype, suppressible by bmmUAS.cUa, Scer\GAL4hs.PB
AMPKαGD736, Scer\GAL4hs.PB has abnormal immune response | adult stage phenotype, suppressible by bmmUAS.cUa, Scer\GAL4hs.PB
AMPKαGD736, Scer\GAL4hs.PB has increased mortality | adult stage | conditional phenotype, suppressible by G6pdUAS.cLa, Scer\GAL4hs.PB
AMPKαGD736, Scer\GAL4hs.PB has abnormal immune response | adult stage phenotype, suppressible by G6pdUAS.cLa, Scer\GAL4hs.PB
AMPKαGD736, Scer\GAL4Ddc.PL is an enhancer of abnormal locomotor behavior | adult stage phenotype of Hsap\LRRK2G2019S.UAS.Tag:MYC, Scer\GAL4Ddc.PL
AMPKαGD736, Scer\GAL4Ddc.PL is a non-enhancer of dopaminergic PPL1 neuron phenotype of Hsap\LRRK2G2019S.UAS.Tag:MYC, Scer\GAL4Ddc.PL
Expression of SNF1AGD736 enhances the climbing defects seen in flies expressing Hsap\LRRK2G2019S.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4Ddc.PL. No further loss of the protocerebral posterior lateral 1 (PPL1) dopaminergic neurons is seen. The beneficial effects of EGCG treatment are completely abolished.