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JNCI Monographs 2008 2008(39):12-15; doi:10.1093/jncimonographs/lgn019
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Published by Oxford University Press 2008.

The RAD5-dependent Postreplication Repair Pathway is Important to Suppress Gross Chromosomal Rearrangements

Kyungjae Myung, Stephanie Smith

Affiliation of authors: Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD

Correspondence to: Kyungjae Myung, PhD, Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Building 49, Room 4A22, Bethesda, MD 20892 (e-mail: kmyung{at}nhgri.nih.gov).

Genome instability is characteristic of cancer cells. Although it frequently occurs during carcinogenesis, the mechanism underlying genome instability is not clearly understood. Recent extensive genetic analyses from different organisms have begun to reveal mechanisms for the suppression of genome instability in general DNA metabolisms including DNA replication, recombination, DNA repair, and signal transduction. One DNA repair pathway called postreplication repair (also known as DNA damage bypass) has been highlighted for its role in genome stability. Central to DNA damage bypass, proliferating cell nuclear antigen (PCNA) directs different pathways through its mono- or polyubiquitination and sumoylation. In this review, we will discuss template switching dictated by the PCNA polyubiquitination and its roles in the suppression of genome instabilities.


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