| 174590 |
Q20748 |
ATAD3_CAEEL |
ATPase family AAA domain-containing protein 3 |
DISRUPTION PHENOTYPE |
RNAi-mediated knockdown results in an increased adult lifespan (PubMed:22245785). RNAi-mediated knockdown at the L1 stage of larval development results in arrest in the majority of animals at this larval stage (PubMed:19888333). Some surviving animals arrest during the subsequent larval stages (PubMed:19888333). RNAi-mediated knockdown in young adults results in a gradual decrease in the reproduction rate over time whereby initially fewer embryos are produced as compared to wild-type animals, and eventually adults fail to reproduce (PubMed:19888333). The few embryos that are produced by the young adults are viable, but animals arrest at the L1 larval stage (PubMed:19888333). RNAi-mediated knockdown results in sufficient mitochondrial function at the L1 larval stage, and no obvious changes in mitochondrial mass (PubMed:19888333). However, RNAi-mediated knockdown results in defects in mitochondrial activity and structure characterized by reduced mitochondrial NADH-ubiquinone oxidoreductase and citrate synthase activity compared to wild-type animals at later stages of development, and a disorganized mitochondrial network with thinner mitochondria (PubMed:19888333). RNAi-mediated knockdown results in increased levels of reactive oxygen species as compared to wild-type animals at 37 degrees Celsius (PubMed:22245785). RNAi-mediated knockdown during early developmental stages and at the L3 larval stage results in increased levels of iron and heme (PubMed:26427876). RNAi-mediated knockdown in a mics-1 mutant background results in an enhanced increase in adult lifespan as compared to the single mutants and wild-type animals (PubMed:22245785). {ECO:0000269|PubMed:19888333, ECO:0000269|PubMed:22245785, ECO:0000269|PubMed:26427876}. |