Radiation-induced cell cycle arrest compromised by p21 deficiency

James Brugarolas, Chitra Chandrasekaran, Jeffrey I. Gordon, David Beach, Tyler Jacks, Gregory J. Hannon

Research output: Contribution to journalLetterpeer-review

1170 Scopus citations


THE protein p21 is a dual inhibitor of cyclin-dependent kinases1-3 and proliferating-cell nuclear antigen (PCNA)4, both of which are required for passage through the cell cycle. The p21 gene is under the transcriptional control of p53 (ref. 5), suggesting that p21 might promote p53-dependent cell cycle arrest or apoptosis. p21 has also been implicated in cell senescence6 and in cell-cycle withdrawal upon terminal differentiation7-9. Here we investigate the role of p21 in these processes using chimaeric mice composed partly of p21 −/− and partly of p21 +/+ cells. Immunohistochemical studies of the p21 +/+ and p21 −/− components of adult small intestine indicated that deletion of p21 had no detectable effect on the migration-associated differentiation of the four principal intestinal epithelial cell lineages or on p53-dependent apoptosis following irradiation. However, p21 −/− mouse embryo fibroblasts are impaired in their ability to undergo Gl arrest following DNA damage.

Original languageEnglish (US)
Pages (from-to)552-557
Number of pages6
Issue number6549
StatePublished - Oct 12 1995

ASJC Scopus subject areas

  • General


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