Abstract
Pseudomonas syringae are Gram-negative, plant pathogenic bacteria that use a type III secretion system (T3SS) to disarm host immune responses and promote bacterial growth within plant tissues. Despite the critical role for type III secretion in promoting virulence, T3SS-encoding genes are not constitutively expressed by P. syringae and must instead be induced during infection. While it has been known for many years that culturing P. syringae in synthetic minimal media can induce the T3SS, relatively little is known about host signals that regulate the deployment of the T3SS during infection. The recent identification of specific plant-derived amino acids and organic acids that induce T3SS-inducing genes in P. syringae has provided new insights into host sensing mechanisms. This review summarizes current knowledge of the regulatory machinery governing T3SS deployment in P. syringae, including master regulators HrpRS and HrpL encoded within the T3SS pathogenicity island, and the environmental factors that modulate the abundance and/or activity of these key regulators. We highlight putative receptors and regulatory networks involved in linking the perception of host signals to the regulation of the core HrpRS–HrpL pathway. Positive and negative regulation of T3SS deployment is also discussed within the context of P. syringae infection, where contributions from distinct host signals and regulatory networks likely enable the fine-tuning of T3SS deployment within host tissues. Last, we propose future research directions necessary to construct a comprehensive model that (a) links the perception of host metabolite signals to T3SS deployment and (b) places these host–pathogen signaling events in the overall context of P. syringae infection.
Highlights
Pseudomonas syringae are Gram-negative, plant pathogenic bacteria that use a type III secretion system (T3SS) to disarm host immune responses and promote bacterial growth within plant tissues
indole-3-acetic acid (IAA) accumulates in P. syringae-infected leaves [90,91,92], T3SS suppression by IAA may enable P. syringae to taper T3SS production in the advanced stages of infection after host immune defenses have been sufficiently disarmed and bacterial growth established in the apoplast [88]
AefR regulon that did not significantly impact T3SS-associated gene expression, the results of this study did support the role of AefR as a genetic regulator of acyl homoserine lactone (AHL) quorum sensing in P. syringae pv. syringae B728a [103]
Summary
Pseudomonas syringae are Gram-negative γ-proteobacteria [1,2] that infect and cause disease in plants, in many cases significantly impacting plant health and agricultural yield [3,4]. The induction of most hrp/hrc genes including hrpL occurred during P. syringae infection of both resistant and susceptible cultivars of host plants [75], as well as during incompatible interactions with nonhost plants [42,79], indicating that the T3SS may be stimulated by signals common among plants rather than host-specific factors. A ten-fold increase in promoter activity of hrpA1, encoding the T3SS pilus protein, was observed in a minimal medium containing tomato exudates relative to phosphate buffer alone, suggesting that soluble plant signals were capable of eliciting T3SS gene expression [70]. These results revealed that the abundance of virulence-inducing signals present during infection is dependent on the plant host genotype and that these chemical signals are important determinants of the outcome of P. syringae–host interactions
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
