The RAD5-dependent postreplication repair pathway is important to suppress gross chromosomal rearrangements.
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.
Myung
Kyungjae
K
Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Building 49, Room 4A22, Bethesda, MD 20892, USA. kmyung@nhgri.nih.gov
Smith
Stephanie
S
D000251:Adenosine Triphosphatases / Q000235:genetics*; D004249:DNA Damage; D004265:DNA Helicases; D004260:DNA Repair; D004261:DNA Replication; D015321:Gene Rearrangement; D005800:Genes, Fungal / Q000502:physiology*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D029701:Saccharomyces cerevisiae Proteins / Q000235:genetics*
D018809:Proliferating Cell Nuclear Antigen; D029701:Saccharomyces cerevisiae Proteins; D000251:Adenosine Triphosphatases; C076225:RAD5 protein, S cerevisiae; D004265:DNA Helicases