Isildar M, Bakale G
Radiat Res. 1985 Sep;103(3):461-5.
In the three (parent-daughter) pairs of Ames Salmonella tester strains TA1535-TA100, TA1537-TA2637, and TA1538-TA98 in which the daughter strains carry the pKM101 plasmid but the parent strains do not, the pKM101 plasmid uniformly confers resistance of the host to uv radiation which indicates that the muc genes of the plasmid are present and function correctly in all three daughter strains. This uniform protection against killing by uv contrasts with the lethality responses of the same parent-daughter pairs to ionizing radiation (ir) where pKM101 again confers lethality protection to TA100 and TA2637 but sensitizes TA98 toward the lethal effects of ir. From these results we conclude that the pathways for error-prone repair of lethal lesions induced by uv and by ionizing radiation are not the same and that the muc genes of the plasmid alone are not sufficient to carry out error-prone repair of lethal lesions induced by ionizing radiation. We infer that a segment of plasmid DNA that is present in TA100 and TA2637 and is required to repair potentially lethal damage induced by ir is deleted in TA98.
