Metabolic Adaptation of <em>Ralstonia solanacearum</em> during Plant Infection: A Methionine Biosynthesis Case Study

<div><p>MetE and MetH are two distinct enzymes that catalyze a similar biochemical reaction during the last step of methionine biosynthesis, MetH being a cobalamin-dependent enzyme whereas MetE activity is cobalamin-independent. In this work, we show that the last step of methionine synthesis in the plant pathogen <em>Ralstonia solanacearum</em> is under the transcriptional control of the master pathogenicity regulator HrpG. This control is exerted essentially on <em>metE</em> expression through the intermediate regulator MetR. Expression of <em>metE</em> is strongly and specifically induced in the presence of plant cells in a <em>hrpG</em>- and <em>metR</em>-dependent manner. <em>metE</em> and <em>metR</em> mutants are not auxotrophic for methionine and not affected for growth inside the plant but produce significantly reduced disease symptoms on tomato whereas disruption of <em>metH</em> has no impact on pathogenicity. The finding that the pathogen preferentially induces <em>metE</em> expression rather than <em>metH</em> in the presence of plant cells is indicative of a probable metabolic adaptation to physiological host conditions since this induction of <em>metE</em> occurs in an environment in which cobalamin, the required co-factor for MetH, is absent. It also shows that MetE and MetH are not functionally redundant and are deployed during specific stages of the bacteria lifecycle, the expression of <em>metE</em> and <em>metH</em> being controlled by multiple and distinct signals.</p>