Deletion of pbpC Enhances Bacterial Pathogenicity on Tomato by Affecting Biofilm Formation, Exopolysaccharides Production, and Exoenzyme Activities in Clavibacter michiganensis

Abstract

Penicillin-binding proteins (PBPs) are considered essential for bacterial peptidoglycan biosynthesis and cell wall assembly. Clavibacter michiganensis is a representative Gram-positive bacterial species that causes bacterial canker in tomato. pbpC plays a significant role in maintaining cell morphological characteristics and stress responses in C. michiganensis. The current study demonstrated that the deletion of pbpC commonly enhances bacterial pathogenicity in C. michiganensis and revealed the mechanisms through which this occurs. The expression of interrelated virulence genes, including celA, xysA, xysB, and pelA, were significantly upregulated in △pbpC mutants. Compared with those in wild-type strains, exoenzyme activities, the formation of biofilm, and the production of exopolysaccharides (EPS) were significantly increased in △pbpC mutants. It is noteworthy that EPS were responsible for the enhancement in bacterial pathogenicity, with the degree of necrotic tomato stem cankers intensifying with the injection of a gradient of EPS from C. michiganensis. These findings highlight new insights into the role of pbpC affecting bacterial pathogenicity, with an emphasis on EPS, advancing the current understanding of phytopathogenic infection strategies for Gram-positive bacteria.

Allelic variations in the chpG effector gene within Clavibacter michiganensis populations determine pathogen host range

“…Unlike many plant-pathogenic gram-negative bacteria, Cm does not possess a type III secretion system capable of delivering effectors directly into host cells. Instead, Cm pathogenicity heavily relies on secreted extracellular hydrolases and apoplastic effectors [ 26 – 29 ]. The main virulence determinants of Cm are encoded within three genomic regions: the pCM1 and pCM2 plasmids and the chp/tomA pathogenicity island (PAI), a 129 kb genomic island localized within the Cm chromosome [ 30 ].…”

Allelic variations in a serine protease effector withinClavibacter michiganensispopulations determine pathogen host range

“…Unlike many plant-pathogenic gram-negative bacteria, Cm does not possess a type III secretion system capable of delivering effectors directly inside hosts cells. Instead, Cm pathogenicity is heavily relies on secreted extracellular hydrolases and apoplastic effectors (26) (27) (28) (29). The main virulence determinants of Cm are encoded within three genomic regions: the pCM1 and pCM2 plasmids and the chp/tomA pathogenicity island (PAI), a 129 kb genomic island localized within the Cm chromosome (30).…”