Tags

Type your tag names separated by a space and hit enter

Replisome structure suggests mechanism for continuous fork progression and post-replication repair.
DNA Repair (Amst) 2019; :102658DR

Abstract

What happens to DNA replication when it encounters a damaged or nicked DNA template has been under investigation for five decades. Initially it was thought that DNA polymerase, and thus the replication-fork progression, would stall at road blocks. After the discovery of replication-fork helicase and replication re-initiation factors by the 1990s, it became clear that the replisome can "skip" impasses and finish replication with single-stranded gaps and double-strand breaks in the product DNA. But the mechanism for continuous fork progression after encountering roadblocks is entangled with translesion synthesis, replication fork reversal and recombination repair. The recently determined structure of the bacteriophage T7 replisome offers the first glimpse of how helicase, primase, leading-and lagging-strand DNA polymerases are organized around a DNA replication fork. The tightly coupled leading-strand polymerase and lagging-strand helicase provides a scaffold to consolidate data accumulated over the past five decades and offers a fresh perspective on how the replisome may skip lesions and complete discontinuous DNA synthesis. Comparison of the independently evolved bacterial and eukaryotic replisomes suggests that repair of discontinuous DNA synthesis occurs post replication in both.

Authors+Show Affiliations

Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD, 20892, USA. Electronic address: weiy@niddk.nih.gov.Laboratory of Molecular Gerontology, National Institute of Aging, National Institutes of Health, 251 Bayview Blvd, Baltimore, MD, 21224, USA.Department of Therapeutic Radiology, Yale University, New Haven, CT, 06520-8040, USA.Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD, 20892, USA.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

31303546

Citation

Yang, Wei, et al. "Replisome Structure Suggests Mechanism for Continuous Fork Progression and Post-replication Repair." DNA Repair, 2019, p. 102658.
Yang W, Seidman MM, Rupp WD, et al. Replisome structure suggests mechanism for continuous fork progression and post-replication repair. DNA Repair (Amst). 2019.
Yang, W., Seidman, M. M., Rupp, W. D., & Gao, Y. (2019). Replisome structure suggests mechanism for continuous fork progression and post-replication repair. DNA Repair, p. 102658. doi:10.1016/j.dnarep.2019.102658.
Yang W, et al. Replisome Structure Suggests Mechanism for Continuous Fork Progression and Post-replication Repair. DNA Repair (Amst). 2019 Jul 8;102658. PubMed PMID: 31303546.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Replisome structure suggests mechanism for continuous fork progression and post-replication repair. AU - Yang,Wei, AU - Seidman,Michael M, AU - Rupp,W Dean, AU - Gao,Yang, Y1 - 2019/07/08/ PY - 2019/7/16/entrez KW - Helicase reload KW - Lesion skipping KW - Polymerase restart KW - Replication fork KW - Replisome SP - 102658 EP - 102658 JF - DNA repair JO - DNA Repair (Amst.) N2 - What happens to DNA replication when it encounters a damaged or nicked DNA template has been under investigation for five decades. Initially it was thought that DNA polymerase, and thus the replication-fork progression, would stall at road blocks. After the discovery of replication-fork helicase and replication re-initiation factors by the 1990s, it became clear that the replisome can "skip" impasses and finish replication with single-stranded gaps and double-strand breaks in the product DNA. But the mechanism for continuous fork progression after encountering roadblocks is entangled with translesion synthesis, replication fork reversal and recombination repair. The recently determined structure of the bacteriophage T7 replisome offers the first glimpse of how helicase, primase, leading-and lagging-strand DNA polymerases are organized around a DNA replication fork. The tightly coupled leading-strand polymerase and lagging-strand helicase provides a scaffold to consolidate data accumulated over the past five decades and offers a fresh perspective on how the replisome may skip lesions and complete discontinuous DNA synthesis. Comparison of the independently evolved bacterial and eukaryotic replisomes suggests that repair of discontinuous DNA synthesis occurs post replication in both. SN - 1568-7856 UR - https://www.unboundmedicine.com/medline/citation/31303546/Replisome_structure_suggests_mechanism_for_continuous_fork_progression_and_post-replication_repair L2 - https://linkinghub.elsevier.com/retrieve/pii/S1568-7864(19)30211-3 DB - PRIME DP - Unbound Medicine ER -