The tumor suppressor gene p53 plays an important role in guarding genomic i
ntegrity. When induced in response to environmental results, the gene produ
ct of p53 functions as a transcription factor to transactivate genes involv
ed in arresting the cell cycle and as a facilitator of DNA repair. In contr
ast, the status of p53 in Chinese hamster ovary (CHO) cells, commonly used
as a model system for various studies including those involving the cell cy
cle and transformation, remains an enigma, In this study, the function and
sequence of p53 in CHO.K1 cells were investigated. The level of p53 protein
s was elevated on ultraviolet (UV) irradiation of the cells, and the protei
ns formed specific complexes as probed with DNA containing p53-binding sequ
ences. Its activities toward responsive promoters were inducible by UV in a
dose-dependent manner. Although p53 in CHO.K1 contained a single missense
mutation at codon 211, the mutation apparently had no effect on the functio
nal properties of the protein. The CHO.K1 cells on X-ray irradiation failed
to arrest at G(1) phase even when the cells were transfected with a wiidty
pe human p53 gene, indicating that the failure probably was not caused by d
ysfunction of its p53, but by some other mechanism. This result is consiste
nt with the finding that p21(Waf1/Cip1) is undetectable in UV-treated CHO.K
1 cells, whereas Gadd45 is induced by UV light in the cells.