DNA replication machinery prevents Rad52-dependent single-strand annealing that leads to gross chromosomal rearrangements at centromeres.


Journal

Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179

Informations de publication

Date de publication:
30 04 2020
Historique:
received: 15 10 2019
accepted: 09 04 2020
entrez: 2 5 2020
pubmed: 2 5 2020
medline: 12 6 2021
Statut: epublish

Résumé

Homologous recombination between repetitive sequences can lead to gross chromosomal rearrangements (GCRs). At fission yeast centromeres, Rad51-dependent conservative recombination predominantly occurs between inverted repeats, thereby suppressing formation of isochromosomes whose arms are mirror images. However, it is unclear how GCRs occur in the absence of Rad51 and how GCRs are prevented at centromeres. Here, we show that homology-mediated GCRs occur through Rad52-dependent single-strand annealing (SSA). The rad52-R45K mutation, which impairs SSA activity of Rad52 protein, dramatically reduces isochromosome formation in rad51 deletion cells. A ring-like complex Msh2-Msh3 and a structure-specific endonuclease Mus81 function in the Rad52-dependent GCR pathway. Remarkably, mutations in replication fork components, including DNA polymerase α and Swi1/Tof1/Timeless, change the balance between Rad51-dependent recombination and Rad52-dependent SSA at centromeres, increasing Rad52-dependent SSA that forms isochromosomes. Our results uncover a role of DNA replication machinery in the recombination pathway choice that prevents Rad52-dependent GCRs at centromeres.

Identifiants

pubmed: 32355220
doi: 10.1038/s42003-020-0934-0
pii: 10.1038/s42003-020-0934-0
pmc: PMC7193609
doi:

Substances chimiques

RAD52 protein, S cerevisiae 0
Rad52 DNA Repair and Recombination Protein 0
Saccharomyces cerevisiae Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

202

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Auteurs

Atsushi T Onaka (AT)

Department of Biological Sciences, Graduate School of Science, Osaka University, 1-1 Machikaneyama, Toyonaka, Osaka, 560-0043, Japan.
Chitose Laboratory Corporation, 2-13-3 Nogawa-honcho, Miyamae-ku, Kawasaki, Kanagawa, 216-0041, Japan.

Jie Su (J)

Department of Biological Sciences, Graduate School of Science, Osaka University, 1-1 Machikaneyama, Toyonaka, Osaka, 560-0043, Japan.

Yasuhiro Katahira (Y)

Department of Biological Sciences, Graduate School of Science, Osaka University, 1-1 Machikaneyama, Toyonaka, Osaka, 560-0043, Japan.
Department of Immunoregulation, Institute of Medical Science, Tokyo Medical University, 6-1-1 Shinjuku-ku, Tokyo, 160-8402, Japan.

Crystal Tang (C)

Department of Biological Sciences, Graduate School of Science, Osaka University, 1-1 Machikaneyama, Toyonaka, Osaka, 560-0043, Japan.

Faria Zafar (F)

Department of Biological Sciences, Graduate School of Science, Osaka University, 1-1 Machikaneyama, Toyonaka, Osaka, 560-0043, Japan.

Keita Aoki (K)

Microbial Physiology Laboratory, Department of Gene Function and Phenomics, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka, 411-8540, Japan.

Wataru Kagawa (W)

Department of Chemistry, Graduate School of Science and Engineering, Meisei University, 2-1-1 Hodokubo, Hino, Tokyo, 191-8506, Japan.

Hironori Niki (H)

Microbial Physiology Laboratory, Department of Gene Function and Phenomics, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka, 411-8540, Japan.

Hiroshi Iwasaki (H)

School of Life Science and Technology, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa, 226-8503, Japan.
Institute of Innovative Research, Tokyo Institute of Technology, 4259 Nagatsuta, Midori-ku, Yokohama, Kanagawa, 226-8503, Japan.

Takuro Nakagawa (T)

Department of Biological Sciences, Graduate School of Science, Osaka University, 1-1 Machikaneyama, Toyonaka, Osaka, 560-0043, Japan. takuro4@bio.sci.osaka-u.ac.jp.

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