Abstract
The contribution of two-hit mutational events to X-ray induced lethal and slow growth mutation in Paramecium aurelia has been estimated by dose rate and fractionation studies. The half-life of the lesions (a) producing the two-hit events is of the order of minutes under log phase conditions, whereas our earlier work shows that the half-life for reparable pre-mutational lesions (b) is of the order of hours. Both types of lesions have longer half lives in stationary phase. Lesion (a) is presumed to be a chromosomal break that can interact to produce chromosomal aberrations. Lesion (b) is presumed to be the reparable precursor of point mutations. Genetic evidence for this identification is not available, however. The relative contribution of these two kinds of lesions to the final mutation will depend on the dose, on the relation of the dose rate to the rate of rejoining of the breaks, and on the rate time available for repair of the precursor of point mutation.