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The  Caenorhabditis elegans  dauer larva is a facultative state of diapause. Mutations affecting dauer signal transduction and morphogenesis have been reported. Of these, most that result in constitutive formation of dauer larvae are temperature-sensitive (ts). The  daf-31  mutant was isolated in genetic screens looking for novel and underrepresented classes of mutants that form dauer and dauer-like larvae non-conditionally. Dauer-like larvae are arrested in development and have some, but not all, of the normal dauer characteristics. We show here that  daf-31  mutants form dauer-like larvae under starvation conditions but are sensitive to SDS treatment. Moreover, metabolism is shifted to fat accumulation in  daf-31  mutants. We cloned the  daf-31  gene and it encodes an ortholog of the arrest-defective-1 protein (ARD1) that is the catalytic subunit of the major N alpha-acetyltransferase (NatA). A  daf-31  promoter::GFP reporter gene indicates  daf-31  is expressed in multiple tissues including neurons, pharynx, intestine and hypodermal cells. Interestingly, overexpression of  daf-31  enhances the longevity phenotype of  daf-2  mutants, which is dependent on the forkhead transcription factor (FOXO) DAF-16. We demonstrate that overexpression of  daf-31  stimulates the transcriptional activity of DAF-16 without influencing its subcellular localization. These data reveal an essential role of NatA in controlling  C. elegans  life history and also a novel interaction between ARD1 and FOXO transcription factors, which may contribute to understanding the function of ARD1 in mammals.

daf-31 Encodes the Catalytic Subunit of N Alpha-Acetyltransferase that Regulates Caenorhabditis elegans Development, Metabolism and Adult Lifespan