Evading plant immunity: feedback control of the T3SS in Pseudomonas syringae
Authors:Christopher Waite1, Jörg Schumacher1, Milija Jovanovic1, Mark Bennett1 and Martin Buck1
doi: 10.15698/mic2017.04.570
Volume 4, pp. 137 to 139, published 17/03/2017.
1 Department of Life Sciences, Imperial College London, UK.
Keywords:
gene regulation, feedback control, T3SS, HrpL, plants, pathogen, Pseudomonas syringae.
Corresponding Author(s):
Conflict of interest statement:
The authors have no conflict of interest to declare in relation to the work presented.
Please cite this article as:
Christopher Waite, Jörg Schumacher, Milija Jovanovic, Mark Bennett and Martin Buck (2017). Evading plant immunity: feedback control of the T3SS in Pseudomonas syringae. Microbial Cell 4(4): 137-139.
© 2017 Waite et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
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.