Ralstonia solanacearum Phc confinement-sensing system is required for slow-killing of the nematode Caenorhabditis elegans.
N. Lynch (1), T. P. DENNY (1) (1) University of Georgia, Athens, GA, USA.
Phytopathology 99:S78 .

Abstract: Many bacteria regulate expression of some genes using quorum-sensing strategies that detect accumulation of extracellular autoinducers. In Ralstonia solanacearum the unique Phc system, which responds to 3-OH PAME, controls a typical acyl-homoserine lactone (AHL) system that regulates expression of one gene (aidA) but otherwise has no known function. Recently, the aidA ortholog in Burkholderia ceonocepacia was shown to be required for slow-killing of Caenorhabditis elegans. We consequently evaluated diverse R. solanacearum wild-type strains and mutants to evaluate their ability to kill C. elegans. Half of the 25 wild-type strains evaluated supported growth of axenic L1 larvae into fertile adults. The other strains, which included AW1, K60 and GMI1000, supported little or no growth and the larvae died. Surprisingly, neither aidA nor the AHL system was essential for toxicity of AW1. The extracellular polysaccharide and the type II and type III protein secretion systems also were nonessential. In contrast, inactivation of phcA, the Phc system global transcriptional regulator, reduced the toxicity of all strains tested. Microscopy revealed that an AW1 variant producing green fluorescent protein colonized the larvae’s digestive tract to a much greater extent than did a comparable phcA mutant. We concluded that PhcA is essential, but not in itself sufficient, for production of unknown factors that improve the ability of R. solanacearum to colonize and slowly kill C. elegans.