Regulation of the Pseudomonas syringae Type III Secretion System by Host Environment Signals

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.

In planta transcriptomics reveals conflicts between pattern-triggered immunity and the AlgU sigma factor regulon

“…The T3SS is a needle-like structure that delivers effector proteins to the plant cell cytoplasm, and is required for Pto virulence [ 8 , 19 ]. Type III effectors (T3Es) are critical for suppressing PTI responses in mock treated plants.…”

“…tomato DC3000 (Pto) [5]. An activated PTI response also restricts Type III effector delivery by Pto and reduces expression of the P. syringae virulence regulon [6][7][8][9]. The early stages of infection are crucial as the pathogen and host compete for Type III Secretion System (T3SS) activation and restriction [6].…”

Plant-Microbe Interaction in Sustainable Agriculture: The Factors That May Influence the Efficacy of PGPM Application

“…On the other hand, the plant can produce proteins that recognize these effectors (or molecules modified by them) and induce a hypersensitivity (HR) response called effector-triggered immunity (ETI) [146]. Despite this, it is reported that through T3SS, bacteria can secrete additional effectors that suppress HR [143,147]. Different rhizobes also present a T3SS [148,149], in addition to the induction of the expression of the nod genes; when NodD is activated by flavonoids, it also upregulates the expression of the transcription factor TtsI, which induces the transcription of T3SS-secreted components and effectors that suppress plant defenses [149,150].…”

Conquering the host: Bordetella spp. and Pseudomonas aeruginosa molecular regulators in lung infection

“…There is mounting evidence that demonstrate that the T3SS in P. aeruginosa , and related Pseudomonas spp. strains, is regulated via QS by an intricate network of bacterial signals that respond to host inflammatory cues ( Pena et al, 2019 ; O’Malley and Anderson, 2021 ).…”