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Dynamic regulation of PCNA ubiquitylation/deubiquitylation
Author(s) -
Fox Jennifer T.,
Lee Kyoo-young,
Myung Kyungjae
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.05.053
Subject(s) - proliferating cell nuclear antigen , ubiquitin , dna replication , dna damage , microbiology and biotechnology , biology , dna , dna repair , genetics , gene
Proliferating Cell Nuclear Antigen (PCNA) ubiquitylation plays a crucial role in maintaining genomic stability during DNA replication. DNA damage stalling the DNA replication fork induces PCNA ubiquitylation that activates DNA damage bypass to prevent the collapse of DNA replication forks that could potentially produce double‐strand breaks and chromosomal rearrangements. PCNA ubiquitylation dictates the mode of bypass depending on the level of ubiquitylation; monoubiquitylation and polyubiquitylation activate error‐prone translesion synthesis and error‐free template switching, respectively. Due to the error‐prone nature of DNA damage bypass, PCNA ubiquitylation needs to be tightly regulated. Here, we review the molecular mechanisms to remove ubiquitin from PCNA including the emerging role of USP1 and ELG1 in this fascinating process.