P53 STATUS, DNA DOUBLE-STRAND BREAK REPAIR PROFICIENCY, AND RADIATIONRESPONSE OF MOUSE LYMPHOID AND MYELOID CELL-LINES

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