FP7Individual fellowship2008–2010

EFFECTOR TARGETS · Host target proteins of Phytophthora secreted effectors

FP7 — People (Marie Curie Actions)

Duration
2008-06-01 → 2010-05-31
EU contribution
€171,092
Participants
1
Scheme
MC-IEF

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Results in brief

Host target proteins of Phytophthora secreted effectors

The oomycete Phytophthora infestans causes late blight, a re-emerging and ravaging disease of potato and tomato. Suppression of host defenses is thought to play a critical role in P. infestans pathogenesis. Nonetheless, host defense suppression by Phytophthora and other eukaryotic pathogens remains poorly understood and only a few pathogen molecules that suppress host defenses have been described. An improved understanding of the molecular basis of host defense suppression will lead to conceptual advances in plant pathology and renewed opportunities for engineering disease resistance in crop plants. Our long-term objective is to dissect the molecular mechanisms that enable oomycete pathogens to successfully infect plants and the plant processes that are perturbed by these pathogens. The overall objective of this proposal was to characterise P. infestans cytoplasmic and nuclear located effectors, and their target host proteins in order to establish the role of these molecules in disease progression. Questions we expected to address, include how effector proteins suppress defence responses; what are their targets in host cells; and how they promote disease. To achive these goals we employed an in vivo co-immunoprecipitation (co-IP) assay to identify the targets of effectors. Among the candidate effector targets, we first focused on the putative targets of the RXLR effector AVRblb2 because of the economical importance of the NB-LRR type R gene 'Rpiblb2' that recognises AVRblb2 and provide broad-spectrum resistance against P. infestans. In this project we show that when expressed in planta RXLR effector AVRblb2 localises at the host cell plasma membrane periphery and focally accumulates around haustoria during P. infestans penetration of host epidermal cells. The unusual accumulation of AVRblb2 around haustoria results in enhanced susceptibility of host plants to P. infestans colonisation. Furthermore, we demonstrate that AVRblb2 targets PLCP C14 and specifically alters its localisation by interfering its secretion into the apoplast. Moreover, secretion of C14 into the apoplast is reduced during P. infestans colonisation on tomato. C14 knockdown via RNAi mediated silencing resulted in enhanced susceptibility towards P. infestans and promoted its hyphal growth.We present compelling evidence that C14 is a novel plant defence protease and its overexpression limits P. infestans infection efficiency. However, this effect can be reverted by AVRblb2. Our data points to an unexpected novel counter defence strategy that plant pathogens utilise at the haustorial interface to neutralise previously unknow defence protease C14. Effectors are great reagents for finding new components of immunity; here AVRblb2 led us to identify a novel immune regulator C14 and a novel pathogen strategy to neutralise host defence proteases. Manipulation of C14 can result in enhanced resistance to P. infestans thus can be used in biotech and breeding. The discovery of AVRblb2 virulence function at haustorial interface, is expected to lead conceptual advances in plant pathology and create new opportunities for engineering durable disease resistance in cultivated plants.

Data: CORDIS, © European Union

Project objective

Oomycete and fungi deliver a variety of effector proteins into plant host cells to suppress defense responses and enable successful colonization. Some of these effectors are secreted into host apoplast where they target plant enzymes to inhibit their activities. Others are secreted into the host cytoplasm and nucleus where they manipulate host immunity. The mechanisms involved in transport of oomycete and fungal effectors and host defense manipulation remain unclear. One key approach to unraveling effector function is to find their host cell targets and derive hypotheses about the effector mode of action. Phytophthora infestans offers an excellent system for applying this strategy. The objective of this proposal is to determine the target proteins of the recently identified family of P. infestans effectors to elucidate their biological function. Our hypothesis is based on the fact that P. infestans secretes a diverse set of proteins that target host proteins to suppress host responses and facilitate infection. This hypothesis is supported by preliminary data that demonstrated that P. infestans RXLR type efector protein, AVR3a, is delivered into the host cytoplasm and suppresses hypersensitive cell death mediated by another Phytophthora protein INF1. In this proposal, we will focus on (i) identification of host interactors of P. infestans cytoplasm and nuclear localized effector proteins; (ii) identification of the functions of host effector targets using a VIGS approach in tomato plants. Considering that none of the host translocated fungal and oomycte effectors have been assigned a precise biological function, the proposed research will provide a significant contribution to understanding how filamentous pathogen effectors promote disease. Also, this proposal will provide insights into key molecular processes regulating susceptibility to an economically important pathogen.

Original text from CORDIS.

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Data: CORDIS, © European Union