3bp deletion resulting in the loss of the second amino acid residue (Leu) from the Akh protein.
Akh1 homozygotes are viable with no obvious morphological defects. The adult flies are slightly but significantly heavier than controls and their survival rate upon starvation is significantly increased compared to controls.
Akh1 has abnormal starvation stress response | adult stage phenotype, enhanceable by mir-137CR
Akh1 has abnormal starvation stress response | adult stage phenotype, enhanceable by mir-137KO
Akh1 has abnormal starvation stress response phenotype, suppressible by AdoR1/AdoR1
Akh1 is an enhancer of abnormal starvation stress response | adult stage | semidominant phenotype of mir-137CR
Akh1 is an enhancer of abnormal starvation stress response | adult stage | semidominant phenotype of mir-137KO
Akh1/Akh1 is a suppressor of abnormal starvation stress response phenotype of AdoR1
AdoR1, Akh1 has abnormal oxidative stress response phenotype
Akh1/Akh1;AdoR1/AdoR1 double mutants have similar mortality rates to wild type flies under starvation conditions. Akh1/Akh1;AdoR1/AdoR1 double mutants have significantly higher mortality rates than controls in response to 20mM paraquat (Akh1/Akh1 single mutants are similar to wild type and AdoR1/AdoR1 single mutants show resistance to paraquat).
Ectopic expression of AkhScer\UAS.cLa under the control of Scer\GAL4Act.PU in the Akh1 mutant background suppresses the increased survival rate of Akh1 adult flies under starvation: the survival rate of AkhScer\UAS.cLa expressing flies is significantly lower than in both Akh1 mutants and wild-type controls.
Akh1 is partially rescued by Scer\GAL4Act.PU/AkhUAS.cLa