Recombination in vivo was studied in recA- heterozygous lacZ merodiploids by performing β-galactosidase assays after infection with λprecA+. Recombination as measured by β-galactosidase production was a linear function of λp ecA+ multiplicity of infection (MOI) when the strain contained a deletion of the chromosomal recA gene. However, when the strain carried a recA1 missense allele, a higher λp recA+ MOI was required to obtain levels of recombination comparable to the Δ(recA) strain, and the slope of the dose-response curve increased to approximately two. It is proposed that negative complementation occurs in mixed tetramers of wild-type and missense recA polypeptides, and that in vivo recombination is a property of a multimeric form of recA protein.
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