Abstract

Microbes are responsible for over 10% of the global yield losses in staple crops such as wheat, rice, and maize. Understanding the decision-making strategies that enable bacterial plant pathogens to evade the host immune system and cause disease is essential for managing their ever growing threat to food security. Many utilise the needle-like type III secretion system (T3SS) to suppress plant immunity, by injecting effector proteins that inhibit eukaryotic signalling pathways into the host cell cytoplasm. Plants can in turn evolve resistance to specific pathogens via recognition and blocking of the T3SS effectors, so leading to an ongoing co-evolutionary ‘arms race’ between pathogen and host pairs. The extracytoplasmic function sigma factor HrpL co-ordinates the expression of the T3SS regulon in the leaf-dwelling Pseudomonas syringae and similar pathogens. Recently, we showed that association of HrpL with a target promoter directly adjacent to the hrpL gene imposes negative autogenous control on its own expression level due to overlapping regulatory elements. Our results suggest that by down-regulating T3SS function, this fine-tuning mechanism enables P. syringae to minimise effector-mediated elicitation of plant immunity.

Highlights

  • The hrp and hrc genes required to build and regulate the T3SS of bacterial plant pathogens, plus many effector loci, are commonly found clustered together in a pathogenicity island

  • The expression of HrpL itself is dependent on the alternative sigma-54 (σ54), necessitating a complex transcription initiation process: a hexameric bacterial enhancer binding protein (EBP) binds the promoter at a distal upstream activation sequence (UAS) before being brought into contact with the inactive RNA polymerase (RNAP)-σ54 holoenzyme via DNA looping

  • In P. syringae, transcription of hrpL is activated by a hetero-hexamer comprising the co-dependent EBPs, HrpR and HrpS, which are thought to respond to currently unknown environmental signals

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Summary

Introduction

The hrp and hrc genes required to build and regulate the T3SS of bacterial plant pathogens, plus many effector loci, are commonly found clustered together in a pathogenicity island. The extracytoplasmic function sigma factor HrpL co-ordinates the expression of the T3SS regulon in the leaf-dwelling Pseudomonas syringae and similar pathogens.

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