The broad-host-range plasmid RK2 encodes three host-lethal kil genes whose actions are controlled by specific kor genes. We have shown previously that the 0' to 5.5' region of RK2 encodes both kilA and korC. Because of the lethal effect of kilA, plasmids with this region cannot be maintained in Escherichia coli unless the RK2 korA gene is also present. To investigate korC in the absence of kilA and therefore of korA, we first mapped kilA and korC to specific segments of the cloned 0' to 5.5' region. This allowed us to construct a korC+ plasmid missing the kilA region and thereby removed the need to have korA in the cell. We found that this korC-encoding plasmid alone is insufficient to control kilC. The korA function is required, and it can be supplied in trans. We also constructed a kilA+ korC- plasmid and found that korA is sufficient to control kilA. Thus, in addition to acting negatively to control kilA, korA acts positively to allow korC control of kilC. This korA dependence of korC is bypassed in a rho-115 mutant of E. coli. We consider the possibility that korA product acts as an antiterminator of transcription in korC expression.