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Intercellular co-ordination of plant defence responses

Reference	BBS/E/J/000C0667
Principal Investigator / Supervisor	Dr Christine Faulkner
Co-Investigators / Co-Supervisors
Institution	John Innes Centre
Department	John Innes Centre Department
Funding type	Research
Value (£)	316,916
Status	Completed
Type	Institute Project
Start date	01/11/2013
End date	31/03/2017
Duration	40 months

Abstract

Plant-pathogen interactions are complex and disease incidence depends on a plant’s’ ability to defend itself against pathogen attack. Plant defence strategies are classified into those triggered by PAMP-triggered immunity (PTI), effector triggered immunity (ETI) and systemic acquired resistance (SAR). Each response involves the generation of high concentrations of small, toxic and mobile molecules, which appear to diffuse from the attack site or synthesis into surrounding cells through plasmodesmata (PD), membrane-lined channels that connect plant cells. This implies that localised pathogen attack can be perceived and trigger responses in surrounding cells unless intercellular connectivity is controlled. In support of this hypothesis, I have shown that chitin associated PTI involves a reduction in intercellular connectivity and communication, a response that is mediated via the chitin receptor LYM2. This highlights a role for symplastic isolation in PTI, possibly serving to concentrate small defence-associated molecules at the attack site and protect the surrounding cells from toxic effects. My work is to determine the role of cell-to-cell connectivity and communication in PTI and also in ETI and SAR. In contrast to PTI, SAR is expected to rely on intercellular connectivity for response generation. I am exploiting lym2 mutants and plants where the PD aperture can be genetically manipulated to determine which responses depend upon cellular isolation and/or on intercellular communication and co-ordination. In these plants I will also monitor the spread of defence associated molecules, e.g., Ca2+ and reactive oxygen species, from the site of attack. This study will form the basis for future work that will exploit PAMP-triggered PD closure to enhance resistance against economically damaging pathogens, which in turn this work will contribute to the developing novel strategies with which plant disease can be controlled and secure food production in changing environments.

Summary

unavailable

Committee	Not funded via Committee
Research Topics	Microbiology, Plant Science
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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