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PERFECTION SIGNED

Probing mechanisms of pathogen effector recognition by plant Resistance proteins to elevate defence gene activation

Total Cost €

0

EC-Contrib. €

0

Partnership

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 PERFECTION project word cloud

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Project "PERFECTION" data sheet

The following table provides information about the project.

Coordinator
THE SAINSBURY LABORATORY 

Organization address
address: Norwich Research Park, Colney Lane
city: NORWICH
postcode: NR47UH
website: http://www.tsl.ac.uk

contact info
title: n.a.
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surname: n.a.
function: n.a.
email: n.a.
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 Coordinator Country United Kingdom [UK]
 Project website http://www.tsl.ac.uk/staff/pingtao-ding/
 Total cost 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-04-01   to  2018-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE SAINSBURY LABORATORY UK (NORWICH) coordinator 183˙454.00

Map

 Project objective

Plant cells tightly regulate gene transcription in response to a changing environment. Stresses, such as pathogen encounters, lead to dramatic transcriptional reprogramming to favor defence activation over basal cellular functions. For effective defence, cells must rapidly alter defence gene mRNA abundance. How extracellular and intracellular recognition of plant pathogens trigger appropriate changes in host mRNA abundance is poorly understood. Upon recognition of pathogen effectors, resistance proteins activate plant defence by unknown mechanisms. My host lab recently reported that the Arabidopsis Resistance gene pair RPS4/RRS1-R elevates expression of certain defence genes, such as those required for salicylic acid biosynthesis, within four hours of detecting PopP2 effector in Arabidopsis. The main goal of this proposal is to understand how effector recognition by RPS4/RRS1-R leads to rapid defence gene induction. We will test the hypothesis that RPS4/RRS1-R proteins directly interact with gene loci that are activated during this process. I will use transgenic Arabidopsis that carry a single genome locus with independently epitope-tagged RPS4, RRS1 and other defence-implicated proteins to investigate: (1) changes in composition of the RPS4/RRS1-R protein complex upon effector recognition using mass spectrometry; (2) effector-induced changes in association of the RPS4/RRS1-R proteins with induced genes using chromatin immunoprecipitation; (3) changes in chromatin status at induced gene regions correlated with gene induction and activation of defence by RPS4/RRS1-R. From this project, I will rigorously test an important model, namely that plant immune receptor complexes directly mediate transcriptional reprogramming of defence genes through chromatin changes upon recognition of effectors. I bring highly complementary expertise in genetics and transcriptional regulation of basal defence from China to Canada and now to TSL that is essential for this project’s success.

 Publications

year authors and title journal last update
List of publications.
2017 Pingtao Ding, Jonathan D.G. Jones
Mis-placed Congeniality: When Pathogens Ask Their Plant Hosts for Another Drink
published pages: 116-117, ISSN: 1534-5807, DOI: 10.1016/j.devcel.2017.01.003
Developmental Cell 40/2 2019-06-13
2017 Sung Un Huh, Volkan Cevik, Pingtao Ding, Zane Duxbury, Yan Ma, Laurence Tomlinson, Panagiotis F. Sarris, Jonathan D. G. Jones
Protein-protein interactions in the RPS4/RRS1 immune receptor complex
published pages: e1006376, ISSN: 1553-7374, DOI: 10.1371/journal.ppat.1006376
PLOS Pathogens 13/5 2019-06-13

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