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First published online September 17, 2008

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The p21-PCNA partnership revisited

PCNA is a master regulator of DNA-synthesis-associated processes, but less is known about its modulators, such as the p21 protein – an inhibitor of cyclin-dependent kinases (CDKs) and PCNA functions. Genotoxic stress induces p21 expression to block cell-cycle progression, but UV irradiation results in p21 degradation. The significance of this degradation is unclear, but might be associated with DNA repair. Here, Vanesa Gottifredi and colleagues (p. 3271) address the role of p21 in three PCNA-mediated processes – DNA replication, nucleotide excision repair (NER) and translesion DNA synthesis (TLS). Previous in vitro data suggested that p21 has a major effect on PCNA-driven processes, but the authors show that this is not the case. They find that only the CDK-binding domain of p21 is required to inhibit DNA replication, but neither the CDK-binding nor the PCNA-binding domain can inhibit NER. Interestingly, however, the PCNA-binding domain of p21 inhibits recruitment of the TLS polymerase pol to damaged DNA following UV irradiation, and impairs the assembly of pol foci. Thus, the authors show that p21 is a selective negative regulator of the PCNA-pol interaction, revealing a link between efficient TLS and UV-induced degradation of p21.

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Related articles in JCS:

p21 differentially regulates DNA replication and DNA-repair-associated processes after UV irradiation

Gaston Soria, Juliana Speroni, Osvaldo L. Podhajcer, Carol Prives, and Vanesa Gottifredi
JCS 2008 121: 3271-3282. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?