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Autoimmunity and effector recognition in Arabidopsis thaliana can be uncoupled by mutations in the RRS1-R immune receptor

Title
Autoimmunity and effector recognition in Arabidopsis thaliana can be uncoupled by mutations in the RRS1-R immune receptor
Authors
Toby E. NewmanJungmin LeeSimon J. WilliamsCHOI, SERAMorgan K. HalaneJun ZhouPeter SolomonBostjan KobeJonathan D.G. JonesCécile SegonzacSOHN, KEE HOON
Date Issued
Apr-2019
Publisher
Blackwell Publishing Inc.
Abstract
Plant nucleotide-binding leucine-rich repeat (NLR) disease resistance proteins recognize specific pathogen effectors and activate a cellular defense program. In Arabidopsis thaliana (Arabidopsis), Resistance to Ralstonia solanacearum 1 (RRS1-R) and Resistance to Pseudomonas syringae 4 (RPS4) function together to recognize the unrelated bacterial effectors PopP2 and AvrRps4. In the plant cell nucleus, the RRS1-R/RPS4 complex binds to and signals the presence of AvrRps4 or PopP2. The exact mechanism underlying NLR signaling and immunity activation remains to be elucidated. Using genetic and biochemical approaches, we characterized the intragenic suppressors of sensitive to low humidity 1 (slh1), a temperature-sensitive autoimmune allele of RRS1-R. Our analyses identified five amino acid residues that contribute to RRS1-R-SLH1 autoactivity. We investigated the role of these residues in the RRS1-R allele by genetic complementation, and found that C15 in the Toll/interleukin-1 receptor (TIR) domain and L816 in the LRR domain were also important for effector recognition. Further characterization of the intragenic suppressive mutations located in the RRS1-R TIR domain revealed differing requirements for RRS1-R/RPS4-dependent autoimmunity and effector-triggered immunity. Our results provide novel information about the mechanisms which, in turn, hold an NLR protein complex inactive and allow adequate activation in the presence of pathogens.
URI
http://oasis.postech.ac.kr/handle/2014.oak/94257
ISSN
0028-646X
Article Type
Article
Citation
New Phytologist, vol. 222, no. 2, page. 954 - 965, 2019-04
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 SOHN, KEE HOON
Dept of Life Sciences
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