The meiotic phosphatase GSP-2/PP1 promotes germline immortality and small RNA-mediated genome silencing
Author(s)
Type
Journal Article
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 RNAinduced 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 meiosisspecific 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.
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 RNAinduced 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 meiosisspecific 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.
Date Issued
2019-03-28
Date Acceptance
2019-02-05
Citation
PLoS Genetics, 2019, 15 (3)
ISSN
1553-7390
Publisher
Public Library of Science (PLoS)
Journal / Book Title
PLoS Genetics
Volume
15
Issue
3
Copyright Statement
© 2019 Billmyre et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Sponsor
Medical Research Council
Identifier
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000462994900020&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
Grant Number
MC-A652-5PZ80-3203-0000-0000
Subjects
Science & Technology
Life Sciences & Biomedicine
Genetics & Heredity
C. ELEGANS
GENE-EXPRESSION
HISTONE H3
STEM-CELLS
PIWI
PATHWAY
DROSOPHILA
FERTILITY
SHUGOSHIN
21U-RNAS
Publication Status
Published
Article Number
e1008004
Date Publish Online
2019-03-28