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 beta-galactosidase assays after infection with lambda precA+. Recombination as measured by beta-galactosidase production was a linear function of lambda pecA+ 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 lambda precA+ MOI was required to obtain levels of recombination comparable to the delta (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.