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Defects in Piwi or germ granules trigger a common program of sterility that is independent of transposon activation

Katherine Kretovich Billmyre, Bree Heestand, Maya Spichal, Stephen Frenk, Shawn Ahmed
doi: https://doi.org/10.1101/276782
Katherine Kretovich Billmyre
Department of Genetics, University of North Carolina, Chapel Hill, NC, USADepartment of Biology, University of North Carolina, Chapel Hill, NC, USA
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Bree Heestand
Department of Genetics, University of North Carolina, Chapel Hill, NC, USADepartment of Biology, University of North Carolina, Chapel Hill, NC, USALineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA
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Maya Spichal
Department of Genetics, University of North Carolina, Chapel Hill, NC, USADepartment of Biology, University of North Carolina, Chapel Hill, NC, USA
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Stephen Frenk
Department of Genetics, University of North Carolina, Chapel Hill, NC, USADepartment of Biology, University of North Carolina, Chapel Hill, NC, USA
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Shawn Ahmed
Department of Genetics, University of North Carolina, Chapel Hill, NC, USADepartment of Biology, University of North Carolina, Chapel Hill, NC, USALineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA
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  • For correspondence: shawn@med.unc.edu
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Abstract

Defective Piwi/piRNA genome silencing leads to heterochromatin dysfunction and immediate sterility in many species. Sterile Piwi mutants experience transposon expression and transposon-induced genomic instability, although the cause of Piwi mutant sterility remains uncertain. C. elegans germ cells deficient for Piwi pathway genome silencing factors transmit a form of heritable stress that induces sterility after growth for several generations, allowing comparisons of animals that are close to sterility but fertile with sterile siblings. Sterile Piwi pathway mutants displayed inconsistent increases in DNA damage signaling but consistently altered perinuclear liquid droplets termed germ granules. Germ granule dysfunction did not elicit significant levels of transposon expression but was sufficient to induce a range of idiosyncratic phenotypes associated with sterile Piwi pathway genome silencing mutants, including germline atrophy, reproductive arrest and univalents in oocytes. Expression of genes that perturb germ granule structure was not compromised in sterile Piwi pathway mutants, suggesting that a post-transcriptional mechanism regulates the stability of Piwi mutant germ granules. We propose that sterility in response to transgenerational deficiency for Piwi and in response to acute dysfunction of germ granules occur as a consequence of a common reproductive arrest mechanism. The germ granule abnormalities of sterile Piwi pathway mutants therefore suggest germ granule dysfunction as a cause of Piwi mutant sterility.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted August 07, 2018.
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Defects in Piwi or germ granules trigger a common program of sterility that is independent of transposon activation
Katherine Kretovich Billmyre, Bree Heestand, Maya Spichal, Stephen Frenk, Shawn Ahmed
bioRxiv 276782; doi: https://doi.org/10.1101/276782
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Defects in Piwi or germ granules trigger a common program of sterility that is independent of transposon activation
Katherine Kretovich Billmyre, Bree Heestand, Maya Spichal, Stephen Frenk, Shawn Ahmed
bioRxiv 276782; doi: https://doi.org/10.1101/276782

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