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Smooth muscle (sm) a-actin is expressed in vascular smooth muscle cells and ®broblast cells. Its expression is regulated by cell proliferation and repressed during oncogenic transformation. In this study, we demonstrate that p53 activation is associated with a dramatic increase in organized micro®lament bundles and an increase in sm a-actin mRNA level. Wild-type p53, but not mutant p53, strongly stimulated human sm a-actin promoter activity in p53 null cell lines. The sequences homologous to the p53 consensus sequence and to the p53 binding sequence from the muscle creatine kinase, were found within a speci®c region of the sm a-actin promoter. This sequence was su cient to confer p53-dependent activation to a heterologous promoter and p53 was capable of binding to this sequence as assessed by gel shift analysis. Ionizing irradiation of colorectal tumor cells caused an increase in a-actin mRNA level in a p53-dependent manner. Taken together, these results demonstrate that human sm aactin gene is a transcriptional target for p53 tumor suppressor protein and represents the ®rst example of a cytoskeletal gene with a functionally de®ned p53 response element.

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