Loading…
Matching NLR Immune Receptors to Autoimmunity in camta3 Mutants Using Antimorphic NLR Alleles
To establish infection, pathogens deploy effectors to modify or remove host proteins. Plant immune receptors with nucleotide-binding, leucine-rich repeat domains (NLRs) detect these modifications and trigger immunity. Plant NLRs thus guard host “guardees.” A corollary is that autoimmunity may result...
Saved in:
Published in: | Cell host & microbe 2017-04, Vol.21 (4), p.518-529.e4 |
---|---|
Main Authors: | , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c466t-61900444c99a6afd4733eece266e0be7d42b721a4bb8766df4300326e90667993 |
---|---|
cites | cdi_FETCH-LOGICAL-c466t-61900444c99a6afd4733eece266e0be7d42b721a4bb8766df4300326e90667993 |
container_end_page | 529.e4 |
container_issue | 4 |
container_start_page | 518 |
container_title | Cell host & microbe |
container_volume | 21 |
creator | Lolle, Signe Greeff, Christiaan Petersen, Klaus Roux, Milena Jensen, Michael Krogh Bressendorff, Simon Rodriguez, Eleazar Sømark, Kenneth Mundy, John Petersen, Morten |
description | To establish infection, pathogens deploy effectors to modify or remove host proteins. Plant immune receptors with nucleotide-binding, leucine-rich repeat domains (NLRs) detect these modifications and trigger immunity. Plant NLRs thus guard host “guardees.” A corollary is that autoimmunity may result from inappropriate NLR activation because mutations in plant guardees could trigger corresponding NLR guards. To explore these hypotheses, we expressed 108 dominant-negative (DN) Arabidopsis NLRs in various lesion mimic mutants, including camta3, which exhibits autoimmunity. CAMTA3 was previously described as a negative regulator of immunity, and we find that autoimmunity in camta3 is fully suppressed by expressing DNs of two NLRs, DSC1 and DSC2. Additionally, expression of either NLR triggers cell death that can be suppressed by CAMTA3 expression. These findings support a model in which DSC1 and DSC2 guard CAMTA3, and they suggest that other negative regulators of immunity may similarly represent guardees.
[Display omitted]
•Dominant-negative NLR forms (DN-NLR) disrupt the function of wild-type NLR alleles•DN-NLRs can be used to screen for suppression of autoimmunity in autoimmune mutants•Two NLRs (DSC1 and DSC2) are responsible for autoimmunity in Arabidopsis camta3 mutants•Immunity triggered by DSC1 or DSC2 in tobacco is suppressed by CAMTA3 co-expression
NLRs detect pathogen-induced modifications in plant proteins, triggering immunity. Lolle et al. express dominant-negative NLRs (DN-NLRs) and screen for suppressed autoimmunity in various mutants. DN-NLRs for DSC1 and DSC2 suppress autoimmunity in a camta3 mutant, a putative negative regulator of immunity, suggesting that autoimmunity results from detection of modified self. |
doi_str_mv | 10.1016/j.chom.2017.03.005 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1888684200</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1931312817301154</els_id><sourcerecordid>1888684200</sourcerecordid><originalsourceid>FETCH-LOGICAL-c466t-61900444c99a6afd4733eece266e0be7d42b721a4bb8766df4300326e90667993</originalsourceid><addsrcrecordid>eNp9kE1P3DAQhi3Uio9t_wCHysdeEsYf2InEZYUoIC1UQuVYWY4zy3qVxIvtVOLfk7CUIyePrOd9NfMQcsqgZMDU2bZ0m9CXHJguQZQA5wfkmNVCFgpU_eVtZoVgvDoiJyltJ-AcNDskR7ySoGWlj8nfO5vdxg9P9H71QG_7fhyQPqDDXQ4x0RzocszBz_8-v1A_UGf7bAW9G7MdcqKPaQ4vh-z7EHcb796Kll2HHaZv5Ovadgm_v78L8vjr6s_lTbH6fX17uVwVTiqVC8VqACmlq2ur7LqVWgicduBKITSoW8kbzZmVTVNppdq1FACCK6xBKV3XYkF-7nt3MTyPmLLpfXLYdXbAMCbDqqpSleRTakH4HnUxpBRxbXbR9za-GAZm1mq2ZtZqZq0GhJmsTaEf7_1j02P7EfnvcQIu9gBOV_7zGE1yHgeHrY_osmmD_6z_Fch3h_I</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1888684200</pqid></control><display><type>article</type><title>Matching NLR Immune Receptors to Autoimmunity in camta3 Mutants Using Antimorphic NLR Alleles</title><source>BACON - Elsevier - GLOBAL_SCIENCEDIRECT-OPENACCESS</source><creator>Lolle, Signe ; Greeff, Christiaan ; Petersen, Klaus ; Roux, Milena ; Jensen, Michael Krogh ; Bressendorff, Simon ; Rodriguez, Eleazar ; Sømark, Kenneth ; Mundy, John ; Petersen, Morten</creator><creatorcontrib>Lolle, Signe ; Greeff, Christiaan ; Petersen, Klaus ; Roux, Milena ; Jensen, Michael Krogh ; Bressendorff, Simon ; Rodriguez, Eleazar ; Sømark, Kenneth ; Mundy, John ; Petersen, Morten</creatorcontrib><description>To establish infection, pathogens deploy effectors to modify or remove host proteins. Plant immune receptors with nucleotide-binding, leucine-rich repeat domains (NLRs) detect these modifications and trigger immunity. Plant NLRs thus guard host “guardees.” A corollary is that autoimmunity may result from inappropriate NLR activation because mutations in plant guardees could trigger corresponding NLR guards. To explore these hypotheses, we expressed 108 dominant-negative (DN) Arabidopsis NLRs in various lesion mimic mutants, including camta3, which exhibits autoimmunity. CAMTA3 was previously described as a negative regulator of immunity, and we find that autoimmunity in camta3 is fully suppressed by expressing DNs of two NLRs, DSC1 and DSC2. Additionally, expression of either NLR triggers cell death that can be suppressed by CAMTA3 expression. These findings support a model in which DSC1 and DSC2 guard CAMTA3, and they suggest that other negative regulators of immunity may similarly represent guardees.
[Display omitted]
•Dominant-negative NLR forms (DN-NLR) disrupt the function of wild-type NLR alleles•DN-NLRs can be used to screen for suppression of autoimmunity in autoimmune mutants•Two NLRs (DSC1 and DSC2) are responsible for autoimmunity in Arabidopsis camta3 mutants•Immunity triggered by DSC1 or DSC2 in tobacco is suppressed by CAMTA3 co-expression
NLRs detect pathogen-induced modifications in plant proteins, triggering immunity. Lolle et al. express dominant-negative NLRs (DN-NLRs) and screen for suppressed autoimmunity in various mutants. DN-NLRs for DSC1 and DSC2 suppress autoimmunity in a camta3 mutant, a putative negative regulator of immunity, suggesting that autoimmunity results from detection of modified self.</description><identifier>ISSN: 1931-3128</identifier><identifier>EISSN: 1934-6069</identifier><identifier>DOI: 10.1016/j.chom.2017.03.005</identifier><identifier>PMID: 28407487</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Alleles ; Arabidopsis - immunology ; Arabidopsis Proteins - genetics ; Arabidopsis Proteins - metabolism ; Autoimmunity ; Mutant Proteins - genetics ; Mutant Proteins - metabolism ; NLR Proteins - genetics ; NLR Proteins - metabolism ; Transcription Factors - genetics ; Transcription Factors - metabolism</subject><ispartof>Cell host & microbe, 2017-04, Vol.21 (4), p.518-529.e4</ispartof><rights>2017 Elsevier Inc.</rights><rights>Copyright © 2017 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c466t-61900444c99a6afd4733eece266e0be7d42b721a4bb8766df4300326e90667993</citedby><cites>FETCH-LOGICAL-c466t-61900444c99a6afd4733eece266e0be7d42b721a4bb8766df4300326e90667993</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28407487$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lolle, Signe</creatorcontrib><creatorcontrib>Greeff, Christiaan</creatorcontrib><creatorcontrib>Petersen, Klaus</creatorcontrib><creatorcontrib>Roux, Milena</creatorcontrib><creatorcontrib>Jensen, Michael Krogh</creatorcontrib><creatorcontrib>Bressendorff, Simon</creatorcontrib><creatorcontrib>Rodriguez, Eleazar</creatorcontrib><creatorcontrib>Sømark, Kenneth</creatorcontrib><creatorcontrib>Mundy, John</creatorcontrib><creatorcontrib>Petersen, Morten</creatorcontrib><title>Matching NLR Immune Receptors to Autoimmunity in camta3 Mutants Using Antimorphic NLR Alleles</title><title>Cell host & microbe</title><addtitle>Cell Host Microbe</addtitle><description>To establish infection, pathogens deploy effectors to modify or remove host proteins. Plant immune receptors with nucleotide-binding, leucine-rich repeat domains (NLRs) detect these modifications and trigger immunity. Plant NLRs thus guard host “guardees.” A corollary is that autoimmunity may result from inappropriate NLR activation because mutations in plant guardees could trigger corresponding NLR guards. To explore these hypotheses, we expressed 108 dominant-negative (DN) Arabidopsis NLRs in various lesion mimic mutants, including camta3, which exhibits autoimmunity. CAMTA3 was previously described as a negative regulator of immunity, and we find that autoimmunity in camta3 is fully suppressed by expressing DNs of two NLRs, DSC1 and DSC2. Additionally, expression of either NLR triggers cell death that can be suppressed by CAMTA3 expression. These findings support a model in which DSC1 and DSC2 guard CAMTA3, and they suggest that other negative regulators of immunity may similarly represent guardees.
[Display omitted]
•Dominant-negative NLR forms (DN-NLR) disrupt the function of wild-type NLR alleles•DN-NLRs can be used to screen for suppression of autoimmunity in autoimmune mutants•Two NLRs (DSC1 and DSC2) are responsible for autoimmunity in Arabidopsis camta3 mutants•Immunity triggered by DSC1 or DSC2 in tobacco is suppressed by CAMTA3 co-expression
NLRs detect pathogen-induced modifications in plant proteins, triggering immunity. Lolle et al. express dominant-negative NLRs (DN-NLRs) and screen for suppressed autoimmunity in various mutants. DN-NLRs for DSC1 and DSC2 suppress autoimmunity in a camta3 mutant, a putative negative regulator of immunity, suggesting that autoimmunity results from detection of modified self.</description><subject>Alleles</subject><subject>Arabidopsis - immunology</subject><subject>Arabidopsis Proteins - genetics</subject><subject>Arabidopsis Proteins - metabolism</subject><subject>Autoimmunity</subject><subject>Mutant Proteins - genetics</subject><subject>Mutant Proteins - metabolism</subject><subject>NLR Proteins - genetics</subject><subject>NLR Proteins - metabolism</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><issn>1931-3128</issn><issn>1934-6069</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNp9kE1P3DAQhi3Uio9t_wCHysdeEsYf2InEZYUoIC1UQuVYWY4zy3qVxIvtVOLfk7CUIyePrOd9NfMQcsqgZMDU2bZ0m9CXHJguQZQA5wfkmNVCFgpU_eVtZoVgvDoiJyltJ-AcNDskR7ySoGWlj8nfO5vdxg9P9H71QG_7fhyQPqDDXQ4x0RzocszBz_8-v1A_UGf7bAW9G7MdcqKPaQ4vh-z7EHcb796Kll2HHaZv5Ovadgm_v78L8vjr6s_lTbH6fX17uVwVTiqVC8VqACmlq2ur7LqVWgicduBKITSoW8kbzZmVTVNppdq1FACCK6xBKV3XYkF-7nt3MTyPmLLpfXLYdXbAMCbDqqpSleRTakH4HnUxpBRxbXbR9za-GAZm1mq2ZtZqZq0GhJmsTaEf7_1j02P7EfnvcQIu9gBOV_7zGE1yHgeHrY_osmmD_6z_Fch3h_I</recordid><startdate>20170412</startdate><enddate>20170412</enddate><creator>Lolle, Signe</creator><creator>Greeff, Christiaan</creator><creator>Petersen, Klaus</creator><creator>Roux, Milena</creator><creator>Jensen, Michael Krogh</creator><creator>Bressendorff, Simon</creator><creator>Rodriguez, Eleazar</creator><creator>Sømark, Kenneth</creator><creator>Mundy, John</creator><creator>Petersen, Morten</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20170412</creationdate><title>Matching NLR Immune Receptors to Autoimmunity in camta3 Mutants Using Antimorphic NLR Alleles</title><author>Lolle, Signe ; Greeff, Christiaan ; Petersen, Klaus ; Roux, Milena ; Jensen, Michael Krogh ; Bressendorff, Simon ; Rodriguez, Eleazar ; Sømark, Kenneth ; Mundy, John ; Petersen, Morten</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-61900444c99a6afd4733eece266e0be7d42b721a4bb8766df4300326e90667993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Alleles</topic><topic>Arabidopsis - immunology</topic><topic>Arabidopsis Proteins - genetics</topic><topic>Arabidopsis Proteins - metabolism</topic><topic>Autoimmunity</topic><topic>Mutant Proteins - genetics</topic><topic>Mutant Proteins - metabolism</topic><topic>NLR Proteins - genetics</topic><topic>NLR Proteins - metabolism</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lolle, Signe</creatorcontrib><creatorcontrib>Greeff, Christiaan</creatorcontrib><creatorcontrib>Petersen, Klaus</creatorcontrib><creatorcontrib>Roux, Milena</creatorcontrib><creatorcontrib>Jensen, Michael Krogh</creatorcontrib><creatorcontrib>Bressendorff, Simon</creatorcontrib><creatorcontrib>Rodriguez, Eleazar</creatorcontrib><creatorcontrib>Sømark, Kenneth</creatorcontrib><creatorcontrib>Mundy, John</creatorcontrib><creatorcontrib>Petersen, Morten</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cell host & microbe</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lolle, Signe</au><au>Greeff, Christiaan</au><au>Petersen, Klaus</au><au>Roux, Milena</au><au>Jensen, Michael Krogh</au><au>Bressendorff, Simon</au><au>Rodriguez, Eleazar</au><au>Sømark, Kenneth</au><au>Mundy, John</au><au>Petersen, Morten</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Matching NLR Immune Receptors to Autoimmunity in camta3 Mutants Using Antimorphic NLR Alleles</atitle><jtitle>Cell host & microbe</jtitle><addtitle>Cell Host Microbe</addtitle><date>2017-04-12</date><risdate>2017</risdate><volume>21</volume><issue>4</issue><spage>518</spage><epage>529.e4</epage><pages>518-529.e4</pages><issn>1931-3128</issn><eissn>1934-6069</eissn><abstract>To establish infection, pathogens deploy effectors to modify or remove host proteins. Plant immune receptors with nucleotide-binding, leucine-rich repeat domains (NLRs) detect these modifications and trigger immunity. Plant NLRs thus guard host “guardees.” A corollary is that autoimmunity may result from inappropriate NLR activation because mutations in plant guardees could trigger corresponding NLR guards. To explore these hypotheses, we expressed 108 dominant-negative (DN) Arabidopsis NLRs in various lesion mimic mutants, including camta3, which exhibits autoimmunity. CAMTA3 was previously described as a negative regulator of immunity, and we find that autoimmunity in camta3 is fully suppressed by expressing DNs of two NLRs, DSC1 and DSC2. Additionally, expression of either NLR triggers cell death that can be suppressed by CAMTA3 expression. These findings support a model in which DSC1 and DSC2 guard CAMTA3, and they suggest that other negative regulators of immunity may similarly represent guardees.
[Display omitted]
•Dominant-negative NLR forms (DN-NLR) disrupt the function of wild-type NLR alleles•DN-NLRs can be used to screen for suppression of autoimmunity in autoimmune mutants•Two NLRs (DSC1 and DSC2) are responsible for autoimmunity in Arabidopsis camta3 mutants•Immunity triggered by DSC1 or DSC2 in tobacco is suppressed by CAMTA3 co-expression
NLRs detect pathogen-induced modifications in plant proteins, triggering immunity. Lolle et al. express dominant-negative NLRs (DN-NLRs) and screen for suppressed autoimmunity in various mutants. DN-NLRs for DSC1 and DSC2 suppress autoimmunity in a camta3 mutant, a putative negative regulator of immunity, suggesting that autoimmunity results from detection of modified self.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28407487</pmid><doi>10.1016/j.chom.2017.03.005</doi><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1931-3128 |
ispartof | Cell host & microbe, 2017-04, Vol.21 (4), p.518-529.e4 |
issn | 1931-3128 1934-6069 |
language | eng |
recordid | cdi_proquest_miscellaneous_1888684200 |
source | BACON - Elsevier - GLOBAL_SCIENCEDIRECT-OPENACCESS |
subjects | Alleles Arabidopsis - immunology Arabidopsis Proteins - genetics Arabidopsis Proteins - metabolism Autoimmunity Mutant Proteins - genetics Mutant Proteins - metabolism NLR Proteins - genetics NLR Proteins - metabolism Transcription Factors - genetics Transcription Factors - metabolism |
title | Matching NLR Immune Receptors to Autoimmunity in camta3 Mutants Using Antimorphic NLR Alleles |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-27T09%3A37%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Matching%20NLR%20Immune%20Receptors%20to%20Autoimmunity%20in%20camta3%20Mutants%20Using%20Antimorphic%20NLR%20Alleles&rft.jtitle=Cell%20host%20&%20microbe&rft.au=Lolle,%20Signe&rft.date=2017-04-12&rft.volume=21&rft.issue=4&rft.spage=518&rft.epage=529.e4&rft.pages=518-529.e4&rft.issn=1931-3128&rft.eissn=1934-6069&rft_id=info:doi/10.1016/j.chom.2017.03.005&rft_dat=%3Cproquest_cross%3E1888684200%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c466t-61900444c99a6afd4733eece266e0be7d42b721a4bb8766df4300326e90667993%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1888684200&rft_id=info:pmid/28407487&rfr_iscdi=true |