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PMID: 16687932 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Review

DNA interstrand cross-link repair in the cell cycle: a critical role for polymerase zeta in G1 phase.

Cell cycle (Georgetown, Tex.) ·Vol. 5 ·No. 10 ·2006-05-00 ·Pages 1044-7

McHugh PJ, Sarkar S

Abstract

DNA interstrand cross-links (ICLs) present a formidable challenge to the cellular repair apparatus, but to date ICL repair pathways have proved difficult to dissect genetically. It now appears that this is partly the result of a high degree of cell cycle phase selectivity in the choice of ICL pathway employed. Here we review recent results showing that Polymerase zeta, specialized translesion plays an important role during ICL repair in G1 phase yeast cells, and that PCNA modification by ubiquitin is a key regulator of its activity. Given that this reaction can occur outside the context of S-phase, these results imply a more general role for PCNA modification in the control of DNA repair pathways through the cell cycle, which is dependent on the type of damage or repair intermediate encountered.

MeSH Terms
Cross-Linking Reagents/pharmacology DNA Damage DNA Repair DNA, Fungal/drug effects,metabolism DNA-Directed DNA Polymerase/metabolism G1 Phase Proliferating Cell Nuclear Antigen/metabolism Protein Processing, Post-Translational Saccharomyces cerevisiae Saccharomyces cerevisiae Proteins/metabolism Ubiquitin/metabolism
Chemicals
Cross-Linking Reagents DNA, Fungal Proliferating Cell Nuclear Antigen Saccharomyces cerevisiae Proteins Ubiquitin DNA-Directed DNA Polymerase REV3 protein, S cerevisiae
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
McHugh Peter J
Cancer Research UK Laboratories, Weatherall Institute for Molecular Medicine, University of Oxford, Oxford, UK. [email protected]
Sarkar Sovan
Article Info
Journal
Cell cycle (Georgetown, Tex.)
Abbr.
Cell Cycle
ISSN
1551-4005
Published
2006-05-00
Epub
2006-00-15
Pages
1044-7
Language
English
Region
United States
NLM ID
101137841
Subset
IM
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