Flagella and Pili of Xanthomonas axonopodis pv. glycines are associated with motility,biofilm formation and virulence on soybean

Targeted mutations in flgK, and pilD genes in strain KU‐P‐SW005 of Xanthomonas axonopodis pv. glycines, the cause of pustule disease on soybean, led to altered motility phenotypes. The flgK mutants lacked a monopolar flagellum and lost swimming motility, whereas the pilD mutant lacked type IV pili and was unable to move via twitching, a form of surface motility not previously reported for this pathogen. The flgK and pilD mutants were also altered in biofilm production. The flgK and pilD mutants caused reduced disease in susceptible soybean cultivars Spencer when compared to KU‐P‐SW005. Cell counts of the flgK and pilD mutants on plants remained equivalent to KU‐P‐SW005 10 days after inoculation. Complementation of flgK and pilD mutants restored all phenotypes to wild‐type levels. Therefore, flgK and pilD genes that are required for swimming and twitching motility also affected biofilm formation and virulence on soybean.     

Priming,signaling, and protein production associated with induced resistance by <Emphasis Type="Italic">Bacillus amyloliquefaciens</Emphasis> KPS46

Bacillus amyloliquefaciens KPS46 is a rhizobacterium that induces systemic protection in soybean (Glycine max L.) against several diseases and enhances plant growth. In this study, treatment of soybean seed with KPS46 provided protection to leaves from bacterial pustule, caused by Xanthomonas axonopodis pv. glycines (Xag). KPS46 treatment also increased phenolic content and β-1,3-glucanase and peroxidase activity levels in leaves over non-treated plants. Differential expression of these traits was more rapid and pronounced when KPS46 treated plants were infected with Xag, this pattern indicating priming. Also associated with induced resistance by KPS46 was increased production of salicylic acid (SA) and jasmonic acid (JA) in soybean leaves, suggesting both SA- and JA-dependent signaling pathways are systemically triggered by KPS46 seed treatment. When KPS46 was applied to Arabidopsis roots, however, resistance against Pseudomonas syringae pv. tomato (Pst) was induced only in host genotypes with intact jasmonate, ethylene, and auxin sensitivity. Thus, induced resistance against Pst by KPS46 was SA independent and JA/ethylene dependent. Proteins induced in soybean leaves by KPS46 seed treatment and by the seed treatment in combination with pathogen inoculation were determined by proteomic analysis. Among 20 proteins upregulated in KPS46-treated plants, compared with non-treated plants, only three were defense related. In plants that received both KPS46 treatment and inoculation with Xag, nine of the 20 upregulated protein, as compared with proteins produced Xag inoculated plants having no KPS46 treatment, were defense related. This pattern of increased induction of defense-related proteins following pathogen infection of KPS46 treated plants supported priming by KPS46. Aside from proteins with defense-related function, most of the proteins induced by KPS46 were involved in metabolism and energy conversion, reflecting the strong direct positive effect that KPS46 has on soybean growth.