Nucleotide Excision Repair and Homologous Recombination Systems Commit Differentially to the Repair of DNA-Protein Crosslinks

Toshiaki Nakano; Soh Morishita; Atsushi Katafuchi; Mayumi Matsubara; Yusuke Horikawa; Hiroaki Terato; Amir M.H. Salem; Shunsuke Izumi; Seung Pil Pack; Keisuke Makino; Hiroshi Ide

doi:10.1016/j.molcel.2007.07.029

Nucleotide Excision Repair and Homologous Recombination Systems Commit Differentially to the Repair of DNA-Protein Crosslinks

Toshiaki Nakano, Soh Morishita, Atsushi Katafuchi, Mayumi Matsubara, Yusuke Horikawa, Hiroaki Terato, Amir M.H. Salem, Shunsuke Izumi, Seung Pil Pack, Keisuke Makino, Hiroshi Ide

Research output: Contribution to journal › Article › peer-review

96 Citations (Scopus)

Abstract

DNA-protein crosslinks (DPCs)-where proteins are covalently trapped on the DNA strand-block the progression of replication and transcription machineries and hence hamper the faithful transfer of genetic information. However, the repair mechanism of DPCs remains largely elusive. Here we have analyzed the roles of nucleotide excision repair (NER) and homologous recombination (HR) in the repair of DPCs both in vitro and in vivo using a bacterial system. Several lines of biochemical and genetic evidence show that both NER and HR commit to the repair or tolerance of DPCs, but differentially. NER repairs DPCs with crosslinked proteins of sizes less than 12-14 kDa, whereas oversized DPCs are processed exclusively by RecBCD-dependent HR. These results highlight how NER and HR are coordinated when cells need to deal with unusually bulky DNA lesions such as DPCs.

Original language	English
Pages (from-to)	147-158
Number of pages	12
Journal	Molecular Cell
Volume	28
Issue number	1
DOIs	https://doi.org/10.1016/j.molcel.2007.07.029
Publication status	Published - Oct 12 2007
Externally published	Yes

Keywords

DNA
PROTEINS

ASJC Scopus subject areas

Molecular Biology
Cell Biology

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10.1016/j.molcel.2007.07.029

Cite this

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title = "Nucleotide Excision Repair and Homologous Recombination Systems Commit Differentially to the Repair of DNA-Protein Crosslinks",

abstract = "DNA-protein crosslinks (DPCs)-where proteins are covalently trapped on the DNA strand-block the progression of replication and transcription machineries and hence hamper the faithful transfer of genetic information. However, the repair mechanism of DPCs remains largely elusive. Here we have analyzed the roles of nucleotide excision repair (NER) and homologous recombination (HR) in the repair of DPCs both in vitro and in vivo using a bacterial system. Several lines of biochemical and genetic evidence show that both NER and HR commit to the repair or tolerance of DPCs, but differentially. NER repairs DPCs with crosslinked proteins of sizes less than 12-14 kDa, whereas oversized DPCs are processed exclusively by RecBCD-dependent HR. These results highlight how NER and HR are coordinated when cells need to deal with unusually bulky DNA lesions such as DPCs.",

keywords = "DNA, PROTEINS",

author = "Toshiaki Nakano and Soh Morishita and Atsushi Katafuchi and Mayumi Matsubara and Yusuke Horikawa and Hiroaki Terato and Salem, {Amir M.H.} and Shunsuke Izumi and Pack, {Seung Pil} and Keisuke Makino and Hiroshi Ide",

note = "Funding Information: We thank Bennett Van Houten and Deborah L. Croteau (both NIEHS) for the generous gift of the UvrABC proteins and valuable comments. We are also grateful to Kazuo Yamamoto (Tohoku University), Takehiko Nohmi (NIHS), Masaaki Kanemori (Kanazawa University), Akio Kuroda (Hiroshima University), Marc Bichara (CNRS), Martin G. Marinus (University of Massachusetts), Takashi Hishida and Hideo Shinagawa (both Osaka University), Davor Zahradka (Ruder Boskovic Institute), Benedict Michel (INRA), and the National BioResource Project for the generous gifts of E. coli strains and plasmid. This work was supported in part by Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (to H.I. and K.M.). ",

year = "2007",

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doi = "10.1016/j.molcel.2007.07.029",

language = "English",

volume = "28",

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journal = "Molecular Cell",

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T1 - Nucleotide Excision Repair and Homologous Recombination Systems Commit Differentially to the Repair of DNA-Protein Crosslinks

AU - Nakano, Toshiaki

AU - Morishita, Soh

AU - Katafuchi, Atsushi

AU - Matsubara, Mayumi

AU - Horikawa, Yusuke

AU - Terato, Hiroaki

AU - Salem, Amir M.H.

AU - Izumi, Shunsuke

AU - Pack, Seung Pil

AU - Makino, Keisuke

AU - Ide, Hiroshi

N1 - Funding Information: We thank Bennett Van Houten and Deborah L. Croteau (both NIEHS) for the generous gift of the UvrABC proteins and valuable comments. We are also grateful to Kazuo Yamamoto (Tohoku University), Takehiko Nohmi (NIHS), Masaaki Kanemori (Kanazawa University), Akio Kuroda (Hiroshima University), Marc Bichara (CNRS), Martin G. Marinus (University of Massachusetts), Takashi Hishida and Hideo Shinagawa (both Osaka University), Davor Zahradka (Ruder Boskovic Institute), Benedict Michel (INRA), and the National BioResource Project for the generous gifts of E. coli strains and plasmid. This work was supported in part by Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (to H.I. and K.M.).

PY - 2007/10/12

Y1 - 2007/10/12

N2 - DNA-protein crosslinks (DPCs)-where proteins are covalently trapped on the DNA strand-block the progression of replication and transcription machineries and hence hamper the faithful transfer of genetic information. However, the repair mechanism of DPCs remains largely elusive. Here we have analyzed the roles of nucleotide excision repair (NER) and homologous recombination (HR) in the repair of DPCs both in vitro and in vivo using a bacterial system. Several lines of biochemical and genetic evidence show that both NER and HR commit to the repair or tolerance of DPCs, but differentially. NER repairs DPCs with crosslinked proteins of sizes less than 12-14 kDa, whereas oversized DPCs are processed exclusively by RecBCD-dependent HR. These results highlight how NER and HR are coordinated when cells need to deal with unusually bulky DNA lesions such as DPCs.

AB - DNA-protein crosslinks (DPCs)-where proteins are covalently trapped on the DNA strand-block the progression of replication and transcription machineries and hence hamper the faithful transfer of genetic information. However, the repair mechanism of DPCs remains largely elusive. Here we have analyzed the roles of nucleotide excision repair (NER) and homologous recombination (HR) in the repair of DPCs both in vitro and in vivo using a bacterial system. Several lines of biochemical and genetic evidence show that both NER and HR commit to the repair or tolerance of DPCs, but differentially. NER repairs DPCs with crosslinked proteins of sizes less than 12-14 kDa, whereas oversized DPCs are processed exclusively by RecBCD-dependent HR. These results highlight how NER and HR are coordinated when cells need to deal with unusually bulky DNA lesions such as DPCs.

KW - DNA

KW - PROTEINS

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Nucleotide Excision Repair and Homologous Recombination Systems Commit Differentially to the Repair of DNA-Protein Crosslinks

Abstract

Keywords

ASJC Scopus subject areas

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