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The Caulobacter crescentus histidine kinase genes pleC and divJ have been implicated in the regulation of polar morphogenesis and cell division, respectively. Mutations in pleC also potentiate the cell division phenotype of divJ mutations. To investigate the involvement of the PleC kinase in motility and cell cycle regulation, we carried out a pseudoreversion analysis of the divJ332 allele, which confers a temperature-sensitive motility (Mot ؊ ) phenotype. All cold-sensitive pseudorevertants with a Mot ؉ phenotype at 37°C and a cold-sensitive swarm phenotype in soft agar at 24°C contained extragenic suppressors that were null mutations mapping to pleC. Instead of a cell division defect at the nonpermissive temperature, however, revertants displayed a coldsensitive defect in chemotaxis (Che ؊ ). In addition, the mutant cells were also supermotile, a phenotype previously associated only with mutations in the response regulator gene pleD that block the loss of motility. We also found that the Mot ؊ defect of pleC mutants is suppressed by a pleD301/pleD ؉ merodiploid and results in a similar, supermotile, cold-sensitive Che ؊ phenotype. These results implicate signal transduction pathways mediated by PleC-DivK and DivJ-PleD in the regulation of chemotaxis as well as motility. We discuss these findings and the observation that although the PleC kinase does not play an indispensable role in cell division, a temperature-sensitive allele of pleC (pleC319) has severely reduced viability under stringent growth conditions.

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