Network Rewiring of Homologous Recombination Enzymes during Mitotic Proliferation and Meiosis.
DNA repair
Holliday junction
Mlh1-Mlh3-Exo1
Mph1(FANCM)
Mus81-Mms4(EME1)
Sgs1(BLM)-Top3-Rmi1
Slx1-Slx4(BTDB12)
Srs2(RTEL1)
Yen1(GEN1)
crossing-over
Journal
Molecular cell
ISSN: 1097-4164
Titre abrégé: Mol Cell
Pays: United States
ID NLM: 9802571
Informations de publication
Date de publication:
22 08 2019
22 08 2019
Historique:
received:
22
02
2019
revised:
24
04
2019
accepted:
18
06
2019
pubmed:
29
7
2019
medline:
29
1
2020
entrez:
29
7
2019
Statut:
ppublish
Résumé
Homologous recombination (HR) is essential for high-fidelity DNA repair during mitotic proliferation and meiosis. Yet, context-specific modifications must tailor the recombination machinery to avoid (mitosis) or enforce (meiosis) the formation of reciprocal exchanges-crossovers-between recombining chromosomes. To obtain molecular insight into how crossover control is achieved, we affinity purified 7 DNA-processing enzymes that channel HR intermediates into crossovers or noncrossovers from vegetative cells or cells undergoing meiosis. Using mass spectrometry, we provide a global characterization of their composition and reveal mitosis- and meiosis-specific modules in the interaction networks. Functional analyses of meiosis-specific interactors of MutLγ-Exo1 identified Rtk1, Caf120, and Chd1 as regulators of crossing-over. Chd1, which transiently associates with Exo1 at the prophase-to-metaphase I transition, enables the formation of MutLγ-dependent crossovers through its conserved ability to bind and displace nucleosomes. Thus, rewiring of the HR network, coupled to chromatin remodeling, promotes context-specific control of the recombination outcome.
Identifiants
pubmed: 31351878
pii: S1097-2765(19)30478-2
doi: 10.1016/j.molcel.2019.06.022
pmc: PMC6715774
pii:
doi:
Substances chimiques
Saccharomyces cerevisiae Proteins
0
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
859-874.e4Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM116895
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM137126
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM127029
Pays : United States
Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
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