Ectopic expression of AMPKαK57A.Scer\UAS under the control of Scer\GAL4Ubi.PU results in partial lethality, with majority being viable at 25[o]C but only about a fifth at 30[o]C.
Expression of SNF1AK57A.Scer\UAS under the control of Scer\GAL4109(2)80 results in aberrant morphology in class IV multi-dendritic neurons.
Expression of one or two copies of SNF1AK57A.Scer\UAS under the control of Scer\GAL4Ubi significantly reduces adult lifespan. Co-expression of SNF1AScer\UAS.cMa with SNF1AK57A.Scer\UAS attenuates starvation sensitivity phenotypes.
Heat-shock induced expression of SNF1AK57A.Scer\UAS (under the control of Scer\GAL4hs.PB) in adult stages produces a significant reduction in starvation survival. Starvation sensitivity is indistinguishable in these animals from controls. These animals also exhibit a significant reduction in lifespan under nutrient-rich conditions.
Ubiquitous expression of SNF1AK57A.Scer\UAS (under the control of Scer\GAL4Ubi) results in significantly lower amounts of locomotion during normal, unstressed conditions as compared to controls. However, these flies show an instant increase in activity levels when faced with starvation, as oppose to a steady increase as found in wild-type controls, indicating lower locomotion levels in a fed-state, and elevated locomotion levels in a starvation state.
Total daily food intake is significantly increased in animals expressing SNF1AK57A.Scer\UAS under the control of Scer\GAL4Ubi, independent of nutritional value. Specifically, in both males and females, total dietary intake is nearly twice that of animals with wild-type SNF1A function.
Under fed conditions, larvae expressing SNF1AK57A.Scer\UAS under the control of Scer\GAL4Ubi show significantly more and larger lipid droplets in oenocytes compared to controls, resembling the starved phenotype of wild-type oenocytes.
While there is no overt difference in weight, there is a significant impact of SNF1AK57A.Scer\UAS expression, under the control of Scer\GAL4Ubi, on total triglyceride stores under fed conditions; with the average amount of triglyceride levels for the SNF1AK57A.Scer\UAS flies being significantly lower than control flies.
Measurements of O[[2]] consumption in animals expressing SNF1AK57A.Scer\UAS, under the control of Scer\GAL4Ubi, are consistently higher than in control animals.
Feeding SNF1AK57A.Scer\UAS expressing flies (under the control of Scer\GAL4Ubi) with Rapamycin improves their starvation sensitivity. The median survival of these animals is significantly improved during starvation conditions for females and males.
AMPKαK57A.UAS, Scer\GAL4elav.PU is a suppressor | partially of increased rate of feeding behavior | adult stage phenotype of Hsap\SNCAIPUAS.cLa, Scer\GAL4elav.PU
AMPKαK57A.UAS, Scer\GAL4elav.PU is a suppressor | partially of increased body weight | adult stage phenotype of Hsap\SNCAIPUAS.cLa, Scer\GAL4elav.PU
Scer\GAL4Adss-F71/AMPKαK57A.UAS is a suppressor of long lived phenotype of AdssF71
AMPKαK57A.UAS, Scer\GAL4109(2)80 is a non-suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Scer\GAL4109(2)80, prelUAS.Tag:HA
AMPKαK57A.UAS, Scer\GAL4109(2)80 is a non-suppressor of abdominal dorsal multidendritic neuron ddaC | third instar larval stage phenotype of Scer\GAL4109(2)80, prelUAS.Tag:HA
AMPKαK57A.UAS, Scer\GAL4109(2)80 is a non-suppressor of dendrite | third instar larval stage phenotype of Scer\GAL4109(2)80, prelUAS.Tag:HA
The shortening of the dendritic arbor in class IV ddaC neurons in third instar larvae expressing prelScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4109(2)80 is not significantly affected by co-expression of AMPKαK57A.Scer\UAS.
Expression of SNF1AK57A.Scer\UAS under the control of Scer\GAL4AdSS-F71 suppresses the increased longevity of AdSSF71/+ males and females.
Expression of SNF1AK57A.Scer\UAS enhances the climbing defects seen in flies expressing Hsap\LRRK2G2019S.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4Ddc.PL. The beneficial effects of EGCG treatment on climbing ability are completely abolished. The beneficial effects of AICAR on climbing ability and protocerebral posterior lateral 1 (PPL1) dopaminergic neuron loss are also abolished.
