Xanthomonas axonopodis pathovar citri (Xac) causes bacterial citrus canker, a serious disease of most citrus species.
Xanthomonas campestris pv.
campestris
(
Xcc) is the causal agent of black rot disease in cruciferous plants. In
Xcc, cell-cell signaling is mediated by diffusible signal factor (DSF). Synthesis of DSF depends on RpfB and RpfF. DSF perception and signal transduction have been suggested to involve a two-component system comprising RpfC and RpfG. It has been proposed that these proteins participate in a signal transduction system linking changes in the environment to the synthesis of DSF and the expression of virulence genes. Although the cluster of the rpf genes in
Xac has synteny with the corresponding cluster in
Xcc, two genes (
rpfH and
rpfI) are absent in
Xac. To investigate DSF-mediated regulation during
Xac-
Citrus limon interaction, we constructed two strains of
Xac, one with a mutation in the
rpfF gene, leading to an inability to produce DSF, and one with a mutation in the rpfC gene leading to an overproduction of DSF. These mutants also show decreased levels of extracellular cyclic β-(1,2)-glucans and decreased production of endoglucanase and protease extracellular enzymes. The
Xac DSF-deficient
rpfF and the DSF-hyper producing
rpfC mutants are both severely compromised in their ability to cause canker symptoms in lemon leaves compared to the wild-type. Here we provide evidence that rpf genes in
Xac are involved in controlling virulence factors mediated by DSF.
