Description:
<jats:title>Summary</jats:title><jats:p>The <jats:italic>Acinetobacter calcoaceticus pcaJ</jats:italic> and <jats:italic>catJ</jats:italic> genes, nearly identical in DNA sequence, differ in transcriptional control and are separated by more than 20 kb of chromosomal DNA. The <jats:italic>pcaJ3125</jats:italic> mutation is repaired frequently in organisms containing the wild‐type <jats:italic>catJ</jats:italic> gene. This high‐frequency repair is eliminated in strains iacking the <jats:italic>catJ</jats:italic> gene, which suggests that recombination between the homologous <jats:italic>catJ</jats:italic> and <jats:italic>pcaJ</jats:italic> genes contributes to the high‐frequency repair of the <jats:italic>pcaJ3125</jats:italic> mutation. We report here that the high‐frequency repair also requires a functional <jats:italic>recA</jats:italic> gene. The <jats:italic>A. calcoaceticus recA</jats:italic> gene was cloned in <jats:italic>Escherichia coli</jats:italic> by complementation of a <jats:italic>recA</jats:italic> mutation in the host strain. The nucleotide sequence of a 1506bp DNA fragment containing <jats:italic>A. calcoaceticus recA</jats:italic> was determined. The amino acid sequences of <jats:italic>RecA</jats:italic> from <jats:italic>E. coli and A. calcoaceticus</jats:italic> shared 71% identity. The DNA sequences differed in that a consensus binding site for binding of <jats:italic>LexA</jats:italic> repressor, represented upstream from <jats:italic>recA in E. coli</jats:italic>, is not evident in the corresponding region of the <jats:italic>A. calcoaceticus</jats:italic> DNA sequence. <jats:italic>A Tn5</jats:italic> insertion was introduced into the <jats:italic>A. calcoaceticus recA</jats:italic> gene. Selection for <jats:italic>Tn5</jats:italic>‐encoded kanamycin resistance allowed the inactivated <jats:italic>recA</jats:italic> gene to be recombined by natural transformation into the <jats:italic>A. calcoaceticus</jats:italic> chromosome. Strains that had acquired the mutant gene were sensitive to both MMS and u.v. light, were deficient in natural transformation, and failed to carry out <jats:italic>catJ</jats:italic>‐dependent high‐frequency repair of the <jats:italic>pcaJ3125</jats:italic> mutation.</jats:p>