Negative complementation of recA protein by recA1 polypeptide: in vivo recombination requires a multimeric form of recA protein

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.