Indirect suppression of recB and recC mutations by exonuclease I deficiency.

recB(-)and recC(-) strains of Escherichia coli K12 are recombination deficient and sensitive to ultraviolet light and the drug, mitomycin C. We have reported that sbcB mutations indirectly suppress all three phenotypes and result in the loss of exonuclease I. In this publication we report the occurrence of other mutations that lead to loss of exonuclease I and indirectly suppress mitomycin and UV sensitivity but not recombination deficiency. These mutations (called xonA) are cotransducible with his and closely linked with sbcB. Both sbcB and xonA mutant strains appear to have identical residual amounts of nuclease activity on single-stranded DNA. It is hypothesized that exonuclease I possesses a second activity other than its known ability to degrade single-stranded DNA from a 3'-OH terminus. Accordingly, sbcB mutations would alter the second activity while xonA mutations would not.