摘要：Erwinia tracheiphila is a bacterial plant pathogen that causes a fatal wilt infection in some cucurbit crop plants. Wilt symptoms are thought to be caused by systemic bacterial colonization through xylem that impedes sap flow. However, the genetic determinants of within-plant movement are unknown for this pathogen species. Here, we find that E. tracheiphila has horizontally acquired an operon with a microbial expansin (exlx) gene adjacent to a glycoside hydrolase family 5 (gh5) gene. Plant inoculation experiments with deletion mutants in the individual genes (Δexlx and Δgh5) and the full operon (Δexlx–gh5) resulted in decreased severity of wilt symptoms, decreased mortality rate, and impaired systemic colonization compared to the Wt strain. Co-inoculation experiments with Wt and Δexlx–gh5 rescued the movement defect of the mutant strain, suggesting that expansin and GH5 function extracellularly. Together, these results show that expansin–GH5 contributes to systemic movement through xylem, leading to rapid wilt symptom development and higher rates of plant death. The presence of expansin genes in diverse species of bacterial and fungal wilt-inducing pathogens suggests that microbial expansin proteins may be an under-appreciated virulence factor for many pathogen species.
其他摘要：Abstract Erwinia tracheiphila is a bacterial plant pathogen that causes a fatal wilt infection in some cucurbit crop plants. Wilt symptoms are thought to be caused by systemic bacterial colonization through xylem that impedes sap flow. However, the genetic determinants of within-plant movement are unknown for this pathogen species. Here, we find that E. tracheiphila has horizontally acquired an operon with a microbial expansin ( exlx ) gene adjacent to a glycoside hydrolase family 5 ( gh5 ) gene. Plant inoculation experiments with deletion mutants in the individual genes (Δ exlx and Δ gh5 ) and the full operon (Δ exlx – gh5 ) resulted in decreased severity of wilt symptoms, decreased mortality rate, and impaired systemic colonization compared to the Wt strain. Co-inoculation experiments with Wt and Δ exlx – gh5 rescued the movement defect of the mutant strain, suggesting that expansin and GH5 function extracellularly. Together, these results show that expansin–GH5 contributes to systemic movement through xylem, leading to rapid wilt symptom development and higher rates of plant death. The presence of expansin genes in diverse species of bacterial and fungal wilt-inducing pathogens suggests that microbial expansin proteins may be an under-appreciated virulence factor for many pathogen species.
