Pseudomonas syringae: what it takes to be a pathogen

• Published in: Nature reviews. Microbiology 2018-05, Vol.16 (5), p.316-328
• Main Authors: Xin, Xiu-Fang, Kvitko, Brian, He, Sheng Yang
• Format: Article
• Language: English
• Subjects: 631/326/2565/855; 631/326/41/2531; 631/449/2169/2673; 631/449/2169/597; Analysis; Apoplast; Biological evolution; Ecological monitoring; Environmental conditions; Epidemiology; Gene Expression Regulation, Bacterial; Genetic aspects; Host-Pathogen Interactions; Immunity; Infectious Diseases; Life Sciences; Medical Microbiology; Microbiology; Microbiota; Microorganisms; Parasitology; Pathogens; Phyllosphere; Phylogeny; Plant Diseases - microbiology; Plant-pathogen relationships; Plants - microbiology; Pseudomonas; Pseudomonas syringae; Pseudomonas syringae - genetics; Pseudomonas syringae - pathogenicity; review-article; Virology; Virulence; Virulence (Microbiology)
• ISSN: 1740-1526; 1740-1534
• DOI: 10.1038/nrmicro.2018.17

Key Points Pseudomonas syringae is one of the most common plant pathogens that infect the phyllosphere. P. syringae can live on the plant surface as an epiphyte. To cause disease, it enters the plant, through wounds or natural openings such as stomata, and multiplies within the apoplast. P. syringae is an insightful model for understanding bacterial virulence mechanisms and host adaptation of pathogens as well as microbial evolution, ecology and epidemiology. The P. syringae species complex forms a monophyletic group in the Pseudomonas fluorescens -like division of Pseudomonas . P. syringae strains are split into 13 phylogroups, which separate between early-branching and canonical lineages. Members of the canonical lineages have conserved virulence-associated and phenotypic features and include several plant-specialist phylogroups. P. syringae has also been subdivided into more than 60 pathovars on the basis of host of isolation, host range and other properties. P. syringae attacks plants using a variety of virulence factors, including effector proteins that are translocated into the plant cell via the type III secretion system (T3SS), small-molecule toxins, exopolysaccharides, cell-wall-degrading enzymes and plant hormones (or hormone mimics). Whereas all pathogenic strains of P. syringae possess the T3SS and effectors, they may or may not produce other virulence factors. Plants have evolved a defence mechanism (stomatal closure) to reduce bacterial entry through stomata by detection of pathogen-associated molecular patterns (PAMPs). To defeat stomatal defence, P. syringae uses toxins and T3SS effector proteins to overcome PAMP-induced stomatal closure. Stomatal closure is sensitive to high atmospheric humidity, which could promote bacterial entry into the plant. After entry into the plant, P. syringae encounters the apoplast, a potentially carbohydrate-rich but heavily defended living space for microorganisms. Recent advances in the identification of a minimal repertoire of T3SS effectors and host-mutation-based disease reconstitution experiments provide evidence that immune suppression and establishment of aqueous apoplast are two principal pathogenic processes required for P. syringae growth inside the apoplast. P. syringae infection is profoundly influenced by external environmental conditions, such as air humidity, temperature and microbiota that live on healthy plants. Understanding how abiotic and biotic environmental conditions shape P. syringae i