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A neurosecretory pathway regulates a reversible developmental arrest and metabolic shift at the  Caenorhabditis elegans  dauer larval stage. Defects in an insulin-like signaling pathway cause arrest at the dauer stage. We show here that two  C. elegans Akt/PKB homologs,  akt-1  and  akt-2, transduce insulin receptor-like signals that inhibit dauer arrest and that AKT-1 and AKT-2 signaling are indispensable for insulin receptor-like signaling in  C. elegans.  A loss-of-function mutation in the Fork head transcription factor DAF-16 relieves the requirement for Akt/PKB signaling, which indicates that AKT-1 and AKT-2 function primarily to antagonize DAF-16. This is the first evidence that the major target of Akt/PKB signaling is a transcription factor. An activating mutation in  akt-1, revealed by a genetic screen, as well as increased dosage of wild-type akt-1  relieves the requirement for signaling from AGE-1 PI3K, which acts downstream of the DAF-2 insulin/IGF-1 receptor homolog. This demonstrates that Akt/PKB activity is not necessarily dependent on AGE-1 PI3K activity.  akt-1  and akt-2  are expressed in overlapping patterns in the nervous system and in tissues that are remodeled during dauer formation.

Caenorhabditis elegans Akt/PKB transduces insulin receptor-like signals from AGE-1 PI3 kinase to the DAF-16 transcription factor