Summary: Two mutants of the R plasmid pMG, selected on the basis of loss of enhanced ultraviolet light (u.v.)-induced mutability, no longer protected a wild type, a type mutant, or a type mutant of against the lethal effects of u.v. For one of the R plasmid mutants tested, pPL, a plasmid-determined DNA polymerase was no longer detected. The properties of these mutants support the hypothesis that a plasmid gene function responsible for enhanced u.v.-induced mutability also confers u.v.-protection on the host cells. Furthermore a plasmid-determined DNA polymerase plays a major role in producing these effects.

On the basis of the effects of sodium arsenite on plasmid u.v.-protection and enhanced u.v.-induced mutability in strain , it is proposed that a -dependent, arsenite-sensitive repair pathway is present in .


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