In-frame deletion of sequence encoding the two C-terminal amino acids (DW) of the mature AKH octapeptide, leaving the APRP peptide unaffected.
In-frame deletion of sequence encoding amino acids 28 and 29 (DW) of Akh.
AkhA/AkhA mutants do not display any gross abnormalities in viability, developmental time, female fecundity, body size (measured as length of thorax), adult spontaneous locomotion, flight performance, corpora cardiaca cell number, carbohydrate and lipid stores between L3 and immature adult stages, or carbohydrate stores in mature adults, as compared with controls.
AkhA/AkhA mutants display a significant decrease in hatchability (egg to L1 survival). In the first week of adulthood, AkhA/AkhA mutants develop obesity (significantly increased glyceride to protein ratio), along with increased lipid loading and fat body cell hypertrophy, and significantly decreased circulating sugars in the hemolymph. Adult AkhA/AkhA mutants show impaired climbing performance, slightly increased wing area, significantly increased starvation resistance, impaired lipid (but not carbohydrate) mobilization during starvation, suppressed starvation-induced hyperactivity, increased survival in response to paraquat feeding, but also increased paraquat-induced food aversion, and decreased oxidative stress resistance when assayed by paraquat application directly to the nerve cord, as compared to controls.
AkhA/Akh[+] is a non-enhancer of abnormal starvation stress response | adult stage phenotype of NPFKK111846, Scer\GAL4Tk.PS
AkhA/AkhA is a suppressor of abnormal feeding behavior | adult stage | RU486 conditional phenotype of Scer\GAL4da.Switch.PT, StimRNAi.cEa.UAS
AkhA/Akh[+] is a non-suppressor of abnormal starvation stress response | adult stage phenotype of NPFKK111846, Scer\GAL4Tk.PS