A DNA repair protein and histone methyltransferase interact to promote genome stability in the Caenorhabditis elegans germ line.


Journal

PLoS genetics
ISSN: 1553-7404
Titre abrégé: PLoS Genet
Pays: United States
ID NLM: 101239074

Informations de publication

Date de publication:
02 2019
Historique:
received: 22 06 2018
accepted: 28 01 2019
revised: 06 03 2019
pubmed: 23 2 2019
medline: 29 3 2019
entrez: 23 2 2019
Statut: epublish

Résumé

Histone modifications regulate gene expression and chromosomal events, yet how histone-modifying enzymes are targeted is poorly understood. Here we report that a conserved DNA repair protein, SMRC-1, associates with MET-2, the C. elegans histone methyltransferase responsible for H3K9me1 and me2 deposition. We used molecular, genetic, and biochemical methods to investigate the biological role of SMRC-1 and to explore its relationship with MET-2. SMRC-1, like its mammalian ortholog SMARCAL1, provides protection from DNA replication stress. SMRC-1 limits accumulation of DNA damage and promotes germline and embryonic viability. MET-2 and SMRC-1 localize to mitotic and meiotic germline nuclei, and SMRC-1 promotes an increase in MET-2 abundance in mitotic germline nuclei upon replication stress. In the absence of SMRC-1, germline H3K9me2 generally decreases after multiple generations at high culture temperature. Genetic data are consistent with MET-2 and SMRC-1 functioning together to limit replication stress in the germ line and in parallel to promote other germline processes. We hypothesize that loss of SMRC-1 activity causes chronic replication stress, in part because of insufficient recruitment of MET-2 to nuclei.

Identifiants

pubmed: 30794539
doi: 10.1371/journal.pgen.1007992
pii: PGENETICS-D-18-01292
pmc: PMC6402707
doi:

Substances chimiques

Caenorhabditis elegans Proteins 0
Histones 0
Histone-Lysine N-Methyltransferase EC 2.1.1.43
Met-2 protein, C elegans EC 2.1.1.43
DNA Helicases EC 3.6.4.-
smrc-1 protein, C elegans EC 3.6.4.-

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1007992

Subventions

Organisme : NIH HHS
ID : P40 OD010440
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM089818
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM104007
Pays : United States
Organisme : NIGMS NIH HHS
ID : R15 GM119029
Pays : United States

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Bing Yang (B)

Department of Biology, Syracuse University, Syracuse, New York, United States of America.

Xia Xu (X)

Department of Biology, Syracuse University, Syracuse, New York, United States of America.

Logan Russell (L)

Department of Obstetrics, Gynecology, and Reproductive Sciences, Magee-Womens Research Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.

Matthew T Sullenberger (MT)

Department of Biology, Syracuse University, Syracuse, New York, United States of America.

Judith L Yanowitz (JL)

Department of Obstetrics, Gynecology, and Reproductive Sciences, Magee-Womens Research Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.

Eleanor M Maine (EM)

Department of Biology, Syracuse University, Syracuse, New York, United States of America.

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Classifications MeSH