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: Mia Reeves
    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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