Final Report Summary - EFFECTOR TARGETS (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.
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.