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Deficiency for Piwi results in transmission of a heritable stress that promotes longevity via DAF-16/Foxo

Bree Heestand, Matt Simon, Stephen Frenk, Shawn Ahmed
doi: https://doi.org/10.1101/326769
Bree Heestand
1Department of Genetics, University of North Carolina, Chapel Hill, NC, USA
2Department of Biology, University of North Carolina, Chapel Hill, NC, USA
3Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA
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Matt Simon
1Department of Genetics, University of North Carolina, Chapel Hill, NC, USA
2Department of Biology, University of North Carolina, Chapel Hill, NC, USA
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Stephen Frenk
1Department of Genetics, University of North Carolina, Chapel Hill, NC, USA
2Department of Biology, University of North Carolina, Chapel Hill, NC, USA
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Shawn Ahmed
1Department of Genetics, University of North Carolina, Chapel Hill, NC, USA
2Department of Biology, University of North Carolina, Chapel Hill, NC, USA
3Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA
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Abstract

The C. elegans Piwi Argonaute protein PRG-1 and associated piRNAs protect the genomes of germ cells by suppressing the expression of transposons and potentially deleterious foreign nucleic acids. Deficiency for prg-1 compromises germ cell immortality, resulting in normal fertility for many generations followed by progressively reduced fertility and ultimately sterility. The sterility phenotype of prg-1 mutants was recently shown to be a form of reproductive arrest, which implies that prg-1 mutants may become sterile in response to a form of heritable stress. The DAF-16 stress resistance and longevity factor can promote germ cell immortality of prg-1 mutants by activating a systemic RNAi pathway. We found that this RNAi pathway was not required for the somatic longevity function of DAF-16. Given that prg-1 mutant germ cells may transmit a form of heritable stress, we studied the somatic longevity of prg-1 mutant adults. We found that early generation prg-1 mutants had normal lifespans, but that late-generation adults that displayed reduced fertility or sterility were long lived. Germ cells of long-lived late-generation prg-1 mutants gave rise to F1 cross progeny that were heterozygous for prg-1, fertile and also long lived. However, in the absence of DAF-16, the heritable stress transmitted by prg-1 mutant germ cells was deleterious and caused lifespan to shorten. We conclude that deficiency for the genomic surveillance factor PRG-1/Piwi results in germ cells that transmit a heritable stress that promotes somatic longevity via DAF-16/Foxo, which could be relevant transgenerational regulationof aging.

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Posted May 19, 2018.
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Deficiency for Piwi results in transmission of a heritable stress that promotes longevity via DAF-16/Foxo
Bree Heestand, Matt Simon, Stephen Frenk, Shawn Ahmed
bioRxiv 326769; doi: https://doi.org/10.1101/326769
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Deficiency for Piwi results in transmission of a heritable stress that promotes longevity via DAF-16/Foxo
Bree Heestand, Matt Simon, Stephen Frenk, Shawn Ahmed
bioRxiv 326769; doi: https://doi.org/10.1101/326769

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