Xanthan is not essential for pathogenicity in citrus canker but contributes to Xanthomonas epiphytic survival.

摘要: Xanthan-deficient mutants of Xanthomonas axonopodis pv. citri, the bacterium responsible for citrus canker, were generated by deletion and marker exchange region encoding carboxy-terminal end first glycosyltransferase, GumD. Mutants gumD did not produce xanthan remained pathogenic in plants to same extent as wild-type bacteria. The kinetics appearance initial symptoms, areas plant material affected, growth bacteria inside tissue throughout disease process similar both mutant inoculations. Moreover, exopolysaccharide deficiency impair ability induce hypersensitive response on non-host plants. Apart from variations phenotypic aspects, no differences or survival under different stress conditions observed between xanthan-deficient However, displayed impaired oxidative during stationary phase well epiphytic leaves. Our results suggest that does play an essential role canker at stages infection incompatible interactions X. citri plants, but facilitates maintenance host plant, possibly improving efficiency colonization distant tissue.