Abstract
Pseudomonas syringae is best known as a plant pathogenic bacterium that causes diseases in a multitude of hosts, and it has been used as a model organism to understand the biology of plant disease. Pathogenic and non-pathogenic isolates of P. syringae are also commonly found living as epiphytes and in the wider environment, including water sources such as rivers and precipitation. Ice-nucleating strains of P. syringae are associated with frost damage to crops. The genomes of numerous strains of P. syringae have been sequenced and molecular genetic studies have elucidated many aspects of this pathogen's interaction with its host plants.
Highlights
Graphical abstractThe lifecycle and pathogenicity mechanisms of Pseudomonas syringae. Transmission: P. syringae can be disseminated by rainsplash, aerosols and airborne plant particles (1), insect vectors (2) or as a seed-borne pathogen (3)
Pseudomonas syringae is best known as a plant pathogenic bacterium that causes diseases in a multitude of hosts, and it has been used as a model organism to understand the biology of plant disease
The optimal temperature for growth ranges from 22–30 C, and P. syringae is negative for oxidase and arginine dihydrolase activity
Summary
The lifecycle and pathogenicity mechanisms of Pseudomonas syringae. Transmission: P. syringae can be disseminated by rainsplash, aerosols and airborne plant particles (1), insect vectors (2) or as a seed-borne pathogen (3). Mechanism: P. syringae enters plant tissues through wounds and natural openings such as stomata. Some strains of P. syringae can increase frost damage to plant tissues through ice nucleation promoted by proteins such as InaZ. Pathogen-associated molecular patterns (PAMPs) produced by P. syringae, such as flagellin, are recognized by plant pattern recognition receptors (PRRs), triggering the induction of plant immune responses. P. syringae counters plant immune responses through the production of toxins, and the secretion of effector proteins via a type III secretion system (T3SS). Effector proteins and toxins disable or subvert plant immune responses and alter plant metabolism and physiology to promote P. syringae infection.
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