Abstract
Overproduction of Umu+ or UmuD′ protein by means of a gene carried on a multicopy plasmid suppressed the umuC36 phenotype and permitted induction of mutations by ultraviolet light. The umuC122::Tn5 phenotype was not suppressed. Suppression of the umuC36 phenotype was only seen when excision repair was blocked by acriflavine or by an uvrA or uvrB mutation. Cleavage of UmuD to UmuD′ in SOS-induced cells was not dependent upon the presence of UmuC protein. The results are interpreted in terms of a revised model in which UmuC protein is envisaged as guiding UmuD′ to ReA protein which has recognized and become bound to an appropriate DNA lesion. It is suggested that the umuC36 mutation gives rise to a protein with reduced affinity for UmuD′ and that the effect of this can be compensated by an excess of UmuD′.
Published Version
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