P53 Status, DNA Double-strand Break Repair Proficiency, and Radiation Response of Mouse Lymphoid and Myeloid Cell Lines

Abstract

The p53 status of a panel of 10 mouse lymphoid or myeloid cell lines was determined by immunoprecipitation with mutant- and wild-type-specific antibodies and was compared with the radiation response of the lines. The more rapidly dying cell lines all contained p53 displaying the wild-type epitope. By contrast, four of six more slowly dying cell lines contained either no or mutant p53 protein. It was of interest that radiation-induced apoptosis occurred, albeit at a considerable time after irradiation, in cells ostensibly lacking p53 protein. DNA double-strand break (dsb) repair was examined in both a rapidly and more slowly dying cell line. The rapidly dying cell line was capable of DNA dsb rejoining, however this repair was interrupted by postirradiation DNA degradation.