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Pectobacterium actinidiae is one of the primary pathogens that causes summer canker disease in kiwifruit, yet its pathogenic mechanisms remain unknown. The exopolysaccharide PCAP‐1a, isolated from the fermentation broth of P. actinidiae strain GX1, exhibits notable cytotoxicity and acts as a virulence factor facilitating host infection. Genome‐wide analysis revealed a 21‐gene cluster responsible for the biosynthesis of exopolysaccharides in GX1. Homologous recombination was used to systematically knock out these genes, which led to the identification of RmlA as a key protein in the synthesis of the PCAP‐1a precursor. The deletion of the rmlA gene significantly affected the yield of PCAP‐1a and resulted in a direct reduction in GX1 pathogenicity. Further studies revealed that mutations in the substrate binding site of RmlA weakened its capacity to bind G‐1‐P and dTTP, which led to markedly reduced pathogenicity in the corresponding complemented strains. This study indicates that the exopolysaccharide PCAP‐1a serves as a virulence factor in the pathogenesis of GX1, and its biosynthesis depends on the polysaccharide synthesis gene rmlA and the substrate binding activity of its encoded protein. Deletion of the rmlA gene negatively affected PCAP‐1a yield, structure and directly diminished GX1 pathogenicity. Furthermore, mutations within RmlA's substrate binding site impaired its ability to bind G‐1‐P and dTTP.

Stenotrophomonas maltophilia is emerging as one of the most frequently found bacteria in chronic pulmonary infection. Biofilm is increasingly recognized as a contributing factor to disease pathogenesis. In the present study, a total of 37 isolates of S. maltophilia obtained from chronic pulmonary infection patients were evaluated to the relationship between biofilm production and the relative genes expression. The clonal relatedness of isolates was determined by pulse-field gel electrophoresis. Biofilm formation assays were performed by crystal violet assay, and confirmed by Electron microscopy analysis and CLSM analysis. PCR was employed to learn gene distribution and expression. Twenty-four pulsotypes were designated for 37 S. maltophilia isolates, and these 24 pulsotypes exhibited various levels of biofilm production, 8 strong biofilm-producing S. maltophilia strains with OD492 value above 0.6, 14 middle biofilm-producing strains with OD492 average value of 0.4 and 2 weak biofilm-producing strains with OD492 average value of 0.19. CLSM analysis showed that the isolates from the early stage of chronic infection enable to form more highly structured and multilayered biofim than those in the late stage. The prevalence of spgM, rmlA, and rpfF genes was 83.3%, 87.5%, and 50.0% in 24 S. maltophilia strains, respectively, and the presence of rmlA, spgM or rpfF had a close relationship with biofilm formation but did not significantly affect the mean amount of biofilm. Significant mutations of spgM and rmlA were found in both strong and weak biofilm-producing strains. Mutations in spgM and rmlA may be relevant to biofilm formation in the clinical isolates of S. maltophilia.

The rhamnose-GlcNAc disaccharide is a critical linker which connects arabinogalactan to peptidoglycan via a phosphodiester linkage. The biosynthesis of dTDP-rhamnose is catalysed by four enzymes, and the first reaction is catalysed by an rmlA gene encoding d-glucose-1-phosphate thymidylyltransferase (RmlA). We generated a Mycobacterium smegmatis mc²155 mutant lacking the rmlA gene via a homologous recombination method. We tested the requirement for the rmlA gene and the effect of a lack of RmlA on bacterial cell morphology. The results demonstrate that the rmlA gene is essential for mycobacterial growth and that lack of RmlA activity has profound negative effects on bacterial cell morphology. RmlA is thus a potential target for the development of new antituberculosis drugs.