Distinct roles of XPF-ERCC1 and Rad1-Rad10-Saw1 in replication-coupled and uncoupled inter-strand crosslink repair

Ja-Hwan Seol, Cory Holland, Xiaolei Li, Christopher Kim, Fuyang Li, Melisa Medina-Rivera, Robin Eichmiller, Ignacio F. Gallardo, Ilya J. Finkelstein, Paul Hasty, Eun Yong Shim, Jennifer A. Surtees and Sang Eun Lee ()
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Ja-Hwan Seol: University of Texas Health Science Center at San Antonio
Cory Holland: University of Texas Health Science Center at San Antonio
Xiaolei Li: University of Texas Health Science Center at San Antonio
Christopher Kim: University of Texas Health Science Center at San Antonio
Fuyang Li: University of Texas Health Science Center at San Antonio
Melisa Medina-Rivera: State University of New York
Robin Eichmiller: State University of New York
Ignacio F. Gallardo: The University of Texas at Austin
Ilya J. Finkelstein: The University of Texas at Austin
Paul Hasty: University of Texas Health Science Center at San Antonio
Eun Yong Shim: University of Texas Health Science Center at San Antonio
Jennifer A. Surtees: State University of New York
Sang Eun Lee: University of Texas Health Science Center at San Antonio

Nature Communications, 2018, vol. 9, issue 1, 1-13

Abstract: Abstract Yeast Rad1–Rad10 (XPF–ERCC1 in mammals) incises UV, oxidation, and cross-linking agent-induced DNA lesions, and contributes to multiple DNA repair pathways. To determine how Rad1–Rad10 catalyzes inter-strand crosslink repair (ICLR), we examined sensitivity to ICLs from yeast deleted for SAW1 and SLX4, which encode proteins that interact physically with Rad1–Rad10 and bind stalled replication forks. Saw1, Slx1, and Slx4 are critical for replication-coupled ICLR in mus81 deficient cells. Two rad1 mutations that disrupt interactions between Rpa1 and Rad1–Rad10 selectively disable non-nucleotide excision repair (NER) function, but retain UV lesion repair. Mutations in the analogous region of XPF also compromised XPF interactions with Rpa1 and Slx4, and are proficient in NER but deficient in ICLR and direct repeat recombination. We propose that Rad1–Rad10 makes distinct contributions to ICLR depending on cell cycle phase: in G1, Rad1–Rad10 removes ICL via NER, whereas in S/G2, Rad1–Rad10 facilitates NER-independent replication-coupled ICLR.

Date: 2018
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DOI: 10.1038/s41467-018-04327-0

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