Résumé
Xanthomonas albilineans (Xa) produces albicidin, a unique and specific toxin that causes foliar symptoms of sugarcane leaf scald disease. In X. campestris pv. campestris, a cluster of rpf (for regulation of pathogenicity factors) genes and xanB2 are involved in control of various cellular processes. rpfF and xanB2 encode DSF (diffusible signal factor) and DF (diffusible factor), respectively, which are two quorum sensing signalling molecules. Both quorum sensing systems appear to be used by Xa, since mutation of rpfF in Florida strain XaFL07-1 resulted in reduced protease production, and mutation of xanB2 resulted in loss of xanthomonadin (yellow pigment) production. Mutations of rpfF and xanB2 were verified by PCR analyses. Mutations of rpfF and complementation in trans were also verified by use of an X. campestris DSF reporter strain. Sugarcane cultivar CP80-1743, moderately susceptible to leaf scald, exhibited pencil line symptoms indicative of albicidin production on emerging leaves and colonization of leaf vessels after inoculation of stalks by the decapitation method with all mutants, including separate deletion mutations of rpfG and rpfC (encoding two sensor components of the DSF system). Preliminary experiments indicated that several rpfF and xanB2 mutants colonized sugarcane stalks as efficiently, both spatially and in intensity, as wild type Xa. Additional inoculation experiments are in progress to assess disease severity caused by rpf mutants, including deletion of the entire rpfGCF region. However, our preliminary data showed that neither DSF nor DF is essential for albicidin production or sugarcane colonization by Xa. Therefore, albicidin production and sugarcane colonization by Xa may not be controlled by quorum sensing or may involve another system. (Texte intégral)