The C. elegans Argonaute protein PRG‐1/Piwi and associated piRNAs protect metazoan genomes by silencing transposons and other types of foreign DNA. As prg‐1 mutants are propagated, their fertility deteriorates prior to the onset of a reproductive arrest phenotype that resembles a starvation‐induced stress response. We found that late‐generation prg‐1 mutants with substantially reduced fertility were long‐lived, whereas early‐ or mid‐generation prg‐1 mutants had normal lifespans. Loss of the stress response transcription factor DAF‐16 caused mid‐ or late‐generation prg‐1 mutants to live very short lives, whereas overexpression of DAF‐16 enabled both mid‐ and late‐generation prg‐1 mutants to live long. Cytoplasmic P‐bodies that respond to stress increased in long‐lived late‐generation prg‐1 mutants and were transmitted to F1 but not F2 cross‐progeny. Moreover, moderate levels of heritable stress shorten late‐generation prg‐1 mutant longevity when DAF‐16 or P bodies are deficient. Together, these results suggest that the longevity of late‐generation prg‐1 mutants is a hormetic stress response. However, dauer larvae that occur in response to stress were not observed in late‐generation prg‐1 mutants. Small germ cell nucleoli that depended on germline DAF‐16 were present in late‐generation prg‐1 mutants but were not necessary for their longevity. We propose that prg‐1 mutant germ cells transmit a form of heritable stress, high levels of which promote longevity and strongly reduce fertility. The heritable stress transmitted by prg‐1/Piwi mutant germ cells may be generally relevant to epigenetic inheritance of longevity.
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