ABSTRACT
Xanthomonas citri subsp. citri causes citrus canker disease worldwide in most commercial varieties of citrus. Its transmission occurs mainly by wind-driven rain. Once X. citri reaches a leaf, it can epiphytically survive by forming a biofilm, which enhances the persistence of the bacteria under different environmental stresses and plays an important role in the early stages of host infection. Therefore, the study of genes involved in biofilm formation has been an important step toward understanding the bacterial strategy for survival in and infection of host plants. In this work, we show that the ecnAB toxin-antitoxin (TA) system, which was previously identified only in human bacterial pathogens, is conserved in many Xanthomonas spp. We further show that in X. citri, ecnA is involved in important processes, such as biofilm formation, exopolysaccharide (EPS) production, and motility. In addition, we show that ecnA plays a role in X. citri survival and virulence in host plants. Thus, this mechanism represents an important bacterial strategy for survival under stress conditions.IMPORTANCE Very little is known about TA systems in phytopathogenic bacteria. ecnAB, in particular, has only been studied in bacterial human pathogens. Here, we showed that it is present in a wide range of Xanthomonas sp. phytopathogens; moreover, this is the first work to investigate the functional role of this TA system in Xanthomonas citri biology, suggesting an important new role in adaptation and survival with implications for bacterial pathogenicity.
Subject(s)
Antitoxins/genetics , Citrus/microbiology , Xanthomonas/pathogenicity , Bacterial Proteins/genetics , Bacterial Toxins/genetics , Biofilms/growth & development , Humans , Microbial Viability , Plant Diseases/microbiology , Polysaccharides, Bacterial/metabolism , Quorum Sensing , Virulence , Xanthomonas/metabolism , Xanthomonas/physiologyABSTRACT
Clostridium difficile is an important nosocomial pathogen associated with antibiotic treatments. C. difficile's ability to survive antimicrobial therapy and transition from inert colonization to active infection is one of the most perplexing aspects of C. difficile infections and suggests that additional mechanisms are involved in persistence. In this regard, novel mechanisms linked with pathogenesis and persistence of C. difficile such as toxin-antitoxin systems might significantly contribute to biofilm formation and persistent infection. This review will focus on advances of toxin-antitoxin systems in C. difficile and their putative roles will be discussed.