An ionizing radiation resistant derivative was obtained from the mouse P19H22 (aprt hemizygote) embryonal carcinoma cell line by repeated exposure to 137Cs gamma radiation. Ionizing radiation resistance in the 6Gy-R cell line was not correlated with a failure to undergo cell cycle arrest or a loss of the p53 response after exposure to 137Cs gamma radiation. Moreover, the cells did not display increased resistance to bleomycin, a double strand break inducing agent. However, the cells did display increased resistance to ultraviolet radiation, ethyl methanesulfonate, and 95% oxygen. A mutational analysis demonstrated a > 700fold-fold increase in the frequency of aprt mutants for the 6Gy-R cells, but no change in the frequency of hprt or dhfr mutants. A molecular analysis suggested that the aprt mutations in the 6Gy-R cells arose by recombinational events. A possible association between radiation resistance, DNA repair, and a mutator phenotype for large-scale mutational events is discussed.
|Number of pages||11|
|Journal||Somatic Cell and Molecular Genetics|
|State||Published - Mar 1997|
Bibliographical noteFunding Information:
This work was supl?orted by NIH grants CA56383 (MST) and AG01751 (GMM) and a supplemental grant from NASA (MST). We thank Dr. Rich Cross for help with the p53 analysis. We also thank Dr. Maura Pieretti for a critical reading of this manuscript.
ASJC Scopus subject areas
- Cell Biology