The incidence of recombinational DNA repair and inducible mutagenic DNA repair has been examined in Escherichia coli and 11 related species of enterobacteria. Recombinational repair was found to be a common feature of the DNA repair repertoire of at least 6 genera of enterobacteria. This conclusion is based on observations of (i) damageinduced synthesis of RecA-like proteins, (it) nucleotide hybridization between E. coli recA sequences and some chromosomal DNAs, and (iii) recA-negative complementation by plasmids showing SOS-inducible expression of truncated E. coli recA genes. The mechanism of DNA damage-induced gene expression is therefore sufficiently conserved to allow non-E. coli regulatory elements to govern expression of these cloned truncated E. coli recA genes. In contrast, the process of mutagenic repair, which uses umuC+ umuD+ gene products in E. coli, appeared less widespread. Little ultraviolet lightinduced mutagenesis to rifampicin resistance was detected outside the genus Escherichia, and even within the genus induced mutagenesis was detected in only 3 out of 6 species. Nucleotide hybridization showed that sequences like the E. coli umuCD+ gene are not found in these poorly mutable organisms. Evolutionary questions raised by the sporadic incidence of inducible mutagenic repair are discussed.The SOS system ofEscherichia coli is a sophisticated cellular response to DNA damage and involves induced synthesis of several DNA repair enzymes and changes in the normal cycles of cell division and replication. The key to the integration of these activities is a common transcriptional control mechanism in which expression of at least 17 genes is repressed by LexA A second role of RecA protein is in recombination. This activity is essential for both homologous recombination (6) and the major pathway of postreplication repair (7), which reconstitutes gapped daughter DNA strands by recombinational exchange (8,9). The large effect of this repair on survival is shown by the UV resistance of tsl-l and recA281 lexA mutants, which are repair proficient but do not induce expression of many SOS genes (10-13). Conversely, inhibition of recombination repair by recA-negative complementation causes radiosensitization without inhibiting induction of the SOS genes (14). recA-negative complementation can be caused by cloned truncated recA genes whose products are thought to impair the recombinational activity of chromosomally encoded recA+ protein by subunit mixing.The distinction between recombination repair and mutagenesis is best emphasized by the properties of umuCD mutants (15, 16). These mutants are deficient in mutagenesis induced by agents such as UV and are moderately radiosensitive. However, physical assays show that they are proficient in postreplication repair (17), which, as previously mentioned, is primarily recombinational. Genetic and nucleotide sequence analyses of mutated genes indicate that umuC' and umuD' gene products may act in a tolerance mechanism that permits synthesis of DNA on lesion-conta...

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