Inhibition of bacteriophage lambda development by the klaA gene of broad-host-range plasmid RK2.

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The kil-kor regulon of broad-host-range plasmid RK2 is an unusual array of eight co-regulated operons that express at least 21 genes, including the plasmid replication initiator gene. Some of the operons were first identified as kil loci because uncontrolled expression in the absence of certain kor regulatory genes leads to death of the host cells. The functions of kilA, C and E are unknown, although co-regulation with the replication initiator gene suggests that they may have importance in the maintenance or host range of the plasmid. Here we report studies on the function of klaA, the first of three host-lethal genes in the kilA operon. We found that lambda pklaA-1, a lambda phage containing the klaA gene, is unable to form plaques unless the host expresses the KorA and KorB repressors needed to regulate transcription from the klaA promoter. The failure to form plaques depends on the klaA gene product and results from the inability of infected cells to produce viable phage particles. Transcription of early, delayed early and late genes or processing of lambda DNA are not affected by klaA overexpression, while cell lysis, lambda DNA replication and production of functional phage heads are reduced. However, the failure to produce viable phage is best explained by the inability to synthesize lambda tails. The finding that klaA strongly inhibits a specific morphogenetic step in the assembly of lambda phage particles has significance with respect to the function of klaA on plasmid RK2.