Journal
ANNUAL REVIEW OF PHYTOPATHOLOGY, VOL 51
Volume 51, Issue -, Pages 473-498Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-phyto-082712-102321
Keywords
plant immunity; plant pathogen; type III effector; stomata; plant hormone; pathogenesis
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI060761, R01AI068718] Funding Source: NIH RePORTER
- Howard Hughes Medical Institute Funding Source: Medline
- NIAID NIH HHS [R01AI068718, R01AI060761] Funding Source: Medline
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Since the early 1980s, various strains of the gram-negative bacterial pathogen Pseudomonas syringae have been used as models for understanding plant-bacterial interactions. In 1991, a P. syringae pathovar tomato (Pst) strain, DC3000, was reported to infect not only its natural host tomato but also Arabidopsis in the laboratory, a finding that spurred intensive efforts in the subsequent two decades to characterize the molecular mechanisms by which this strain causes disease in plants. Genomic analysis shows that Pst DC3000 carries a large repertoire of potential virulence factors, including proteinaceous effectors that are secreted through the type III secretion system and a polyketide phytotoxin called coronatine, which structurally mimics the plant hormone jasmonate (JA). Study of Pst DC3000 pathogenesis has not only provided several conceptual advances in understanding how a bacterial pathogen employs type III effectors to suppress plant immune responses and promote disease susceptibility but has also facilitated the discovery of the immune function of stomata and key components of JA signaling in plants. The concepts derived from the study of Pst DC3000 pathogenesis may prove useful in understanding pathogenesis mechanisms of other plant pathogens.
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