Estudio de las bases moleculares de la patogénesis de Xanthomonas axonopodis pv. citri en Citrus limon

FLORENCIA SICILIANO, PABLO TORRES, LORENA SENDÍN, CAROLINA BERMEJO, PAULA FILIPPONE, GABRIEL VELLICE, JACKIE RAMALLO, ATILIO CASTAGNARO, ADRIAN VOJNOV Y MARÍA ROSA MARANO

Buenos Aires, Argentina

Congreso; Baires Biotec 2005, VI Congreso RedBio.; 2005

RedBio

Xanthomonas axonopodis pv. citri (Xac) causes bacterial chancrous a serious disease of citrus. In the related bacterium Xanthomonas campestris pv. campestris (Xcc), the rpfF gene is involved in production of a diffusible extracellular factor (DSF) that positively regulates synthesis of virulence-associated functions like extracellular polysaccharide (EPS) and extracellular enzymes. In addition, in L medium, strains of Xcc carrying mutations in genes within the rpf cluster grew as matrix-enclosed aggregates. DSF perception and signal transduction have been suggested to involve the two-component system comprising RpfC and RpfG. Mutation of rpfC, which encodes the sensor component, leads to over-production of DSF. The addition of DSF can phenotypically restore rpfF but not rpfC mutants to wild type. Two mutants in rpf cluster genes in X. axonopodis pv. citri (Xac) were characterized We demonstrated here that a deletion and kanamicin resistance cassette insertion in the rpfC homolog of Xac, as in Xcc, leads to over-production of DSF. The rpfF mutant instead leaded with no production of these signal molecules. Both, rpfF and rpfC Xac mutant has shown a decreased of periplasmatic and extracellular cyclic ƒÒ-1,2 glucan and the extracellular enzymes endoglucanase and protease  productions. In Leaves of Lemon plants, rpfF and rpfC Xac mutants showed reduced canker symptoms. Supplementation of L medium with DSF (from the rpfC Xac mutant) before bacterial inoculation allowed for dispersed growth of rpfF Xcc mutant but not in rpfC of both Xac and Xcc suggestion similar DSF structure in both pahovarieties. The results suggest that rpf genes  may be involved in controlling virulence factors of Xac and that an inability of production or sensing DSF may be the reason for the virulence deficiency of both Xac mutants.