The beginning of an investigation of the role of recF in the pathways of metabolism of ultraviolet-irradiated DNA in Escherichia coli.

Abstract

The recF gene in Escherichia coli was discovered as a locus of mutations which block recombination in a recB − recC − sbcB − strain but not in a recB + recC + sbcB + strain (Horii and Clark, 1974). To understand the significance which was placed on this result it is necessary to know the functions of the recB, recC, and sbcB genes. The recB and recC genes determine exonuclease V (ExoV), an enzyme whose characteristics have been worked out in several laboratories (see e.g. Goldmark and Linn, 1972). Mutations in these genes inactivate ExoV and produce recombination deficiency (see e.g. Clark, 1973) which can be alleviated by sbcB mutations (Kushner et al., 1971). sbcB is thus a gene whose mutations indirectly suppress the recombination deficiency provoked by the absence of ExoV. The product of the sbcB gene is exonuclease I (ExoI) (Kushner et al., 1971, Yajko et al., 1974), an enzyme which degrades single-stranded DNA from 3′-OH termini (Lehman and Nussbaum, 1964). In recB − recC − strains it is presumably the inactivation of ExoI by sbcB mutations which leads to recombination ability, while it is the presence of ExoI which produces recombination deficiency. To explain this, Horii and Clark (1974) hypothesized a pathway of recombination normally inhibited by ExoI which was released from inhibition by the sbcB mutations. This pathway, called the RecF pathway after the recF gene, was considered to be independent of the pathway of recombination involving the recB and recC genes, the RecBC pathway.