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PLoS Genet. 2019 Mar 28;15(3):e1008004. doi: 10.1371/journal.pgen.1008004. eCollection 2019 Mar.

The meiotic phosphatase GSP-2/PP1 promotes germline immortality and small RNA-mediated genome silencing.

Author information

1
Department of Genetics, University of North Carolina, Chapel Hill, North Carolina, United States of America.
2
Department of Biology, University of North Carolina, Chapel Hill, North Carolina, United States of America.
3
Department of Genetics, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
4
Medical Research Council London Institute of Medical Sciences, London, United Kingdom.
5
Institute for Clinical Sciences, Imperial College London, London, United Kingdom.
6
Graduate school of Biostudies, Kyoto University, Kyoto, Japan.
7
Department of Zoology, University of British Columbia, Vancouver, British Columbia, Canada.

Abstract

Germ cell immortality, or transgenerational maintenance of the germ line, could be promoted by mechanisms that could occur in either mitotic or meiotic germ cells. Here we report for the first time that the GSP-2 PP1/Glc7 phosphatase promotes germ cell immortality. Small RNA-induced genome silencing is known to promote germ cell immortality, and we identified a separation-of-function allele of C. elegans gsp-2 that is compromised for germ cell immortality and is also defective for small RNA-induced genome silencing and meiotic but not mitotic chromosome segregation. Previous work has shown that GSP-2 is recruited to meiotic chromosomes by LAB-1, which also promoted germ cell immortality. At the generation of sterility, gsp-2 and lab-1 mutant adults displayed germline degeneration, univalents, histone methylation and histone phosphorylation defects in oocytes, phenotypes that mirror those observed in sterile small RNA-mediated genome silencing mutants. Our data suggest that a meiosis-specific function of GSP-2 ties small RNA-mediated silencing of the epigenome to germ cell immortality. We also show that transgenerational epigenomic silencing at hemizygous genetic elements requires the GSP-2 phosphatase, suggesting a functional link to small RNAs. Given that LAB-1 localizes to the interface between homologous chromosomes during pachytene, we hypothesize that small localized discontinuities at this interface could promote genomic silencing in a manner that depends on small RNAs and the GSP-2 phosphatase.

PMID:
30921322
PMCID:
PMC6456222
DOI:
10.1371/journal.pgen.1008004
[Indexed for MEDLINE]
Free PMC Article

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