p63 and p73 are required for p53-dependent apoptosis in response to DNA damage

Elsa R. Flores, Kenneth Y. Tsai, Denise Crowley, Shomit Sengupta, Annie Yang, Frank McKeon and Tyler Jacks ()
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Elsa R. Flores: Massachusetts Institute of Technology, Department of Biology and Center for Cancer Research
Kenneth Y. Tsai: Massachusetts Institute of Technology, Department of Biology and Center for Cancer Research
Denise Crowley: Massachusetts Institute of Technology, Department of Biology and Center for Cancer Research
Shomit Sengupta: Massachusetts Institute of Technology, Department of Biology and Center for Cancer Research
Annie Yang: Harvard Medical School
Frank McKeon: Harvard Medical School
Tyler Jacks: Massachusetts Institute of Technology, Department of Biology and Center for Cancer Research

Nature, 2002, vol. 416, issue 6880, 560-564

Abstract: Abstract The tumour-suppressor gene p53 is frequently mutated in human cancers and is important in the cellular response to DNA damage1,2. Although the p53 family members p63 and p73 are structurally related to p53, they have not been directly linked to tumour suppression, although they have been implicated in apoptosis3,4,5,6,7,8,9. Given the similarity between this family of genes and the ability of p63 and p73 to transactivate p53 target genes10,11, we explore here their role in DNA damage-induced apoptosis. Mouse embryo fibroblasts deficient for one or a combination of p53 family members were sensitized to undergo apoptosis through the expression of the adenovirus E1A oncogene12,13,14. While using the E1A system facilitated our ability to perform biochemical analyses, we also examined the functions of p63 and p73 using an in vivo system in which apoptosis has been shown to be dependent on p53. Using both systems, we show here that the combined loss of p63 and p73 results in the failure of cells containing functional p53 to undergo apoptosis in response to DNA damage.

Date: 2002
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DOI: 10.1038/416560a

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