STRUCTURE-FUNCTION STUDIES OF TRANSLOCATED EFFECTORS FROM THE LATE BLIGHT PATHOGEN

King, Stuart (2013) STRUCTURE-FUNCTION STUDIES OF TRANSLOCATED EFFECTORS FROM THE LATE BLIGHT PATHOGEN. Doctoral thesis, University of East Anglia.

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Abstract

An almost universal feature of successful pathogens is the secretion of effector
proteins, many of which translocate inside host cells. These effectors manipulate
host processes for the pathogen’s benefit. However, in response to this manipulation,
plants have evolved to monitor for effectors and trigger defence responses.
Amongst plant pathogens, oomycetes of the genus Phytophthora have arguably
caused almost unrivalled levels of human suffering and represent significant threats
to global food security. The late blight pathogen, Phytophthora infestans, is the most
devastating pathogen of potato – the fourth most important food crop worldwide.
Effective and durable resistance against late blight is desperately needed; and will
depend on an improved understanding of the mechanistic basis of disease.
Determining the adaptive functions of effectors might reveal previously unexploited
management strategies.
This work details structure-function studies of two translocated effectors from the
late blight pathogen; PexRD2, a representative RXLR effector, and CRN8, an
effector with kinase activity. Efforts to heterologously express CRN8 were hampered
by protein insolubility and low yields. However, the crystal structure of PexRD2
revealed that it homodimerises, and was crucial to the discovery of a conserved
oomycete effector protein fold, the WY-domain fold.
Yeast two-hybrid screening identified four PexRD2-interacting host proteins,
including MAPKKKε, a known positive regulator of plant immunity. MAP-kinase
cascades transduce the perception of invading pathogens into effective defence
responses, and MAPKKKε is involved in resistance against P. infestans. PexRD2
specifically suppresses cell deaths that are either MAPKKKε-dependent or triggered
by MAPKKKε overexpression. PexRD2 also inhibits MAPKKKε-triggered MAPK
activation. Further, structure-led mutagenesis of PexRD2 suggests that this effector
benefits the pathogen by interacting with MAPKKKε to inhibit the kinase’s
signalling. Discovering the PexRD2-MAPKKKε interaction, and its implications for
plant immunity, has suggested unexploited management strategies that could
enhance crop resistance to this devastating pathogen.

Item Type:	Thesis (Doctoral)
Faculty \ School:	Faculty of Science > School of Biological Sciences
Depositing User:	Users 2259 not found.
Date Deposited:	11 Mar 2014 14:55
Last Modified:	17 Dec 2014 01:38
URI:	https://ueaeprints.uea.ac.uk/id/eprint/48079
DOI:

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