An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis

Plant intracellular NLR receptors recognise pathogen interference to trigger immunity but how NLRs signal is not known. Enhanced disease susceptibility1 (EDS1) heterodimers are recruited by Toll-interleukin1-receptor domain NLRs (TNLs) to transcriptionally mobilise resistance pathways. By interrogat...

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Autores principales: Bhandari, Deepak D., Lapin, Dmitry, Kracher, Barbara, von Born, Patrick, Bautor, Jaqueline, Niefind, Karsten, Parker, Jane E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
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Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6377607/
https://www.ncbi.nlm.nih.gov/pubmed/30770836
http://dx.doi.org/10.1038/s41467-019-08783-0
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author Bhandari, Deepak D.
Lapin, Dmitry
Kracher, Barbara
von Born, Patrick
Bautor, Jaqueline
Niefind, Karsten
Parker, Jane E.
author_facet Bhandari, Deepak D.
Lapin, Dmitry
Kracher, Barbara
von Born, Patrick
Bautor, Jaqueline
Niefind, Karsten
Parker, Jane E.
author_sort Bhandari, Deepak D.
collection PubMed
description Plant intracellular NLR receptors recognise pathogen interference to trigger immunity but how NLRs signal is not known. Enhanced disease susceptibility1 (EDS1) heterodimers are recruited by Toll-interleukin1-receptor domain NLRs (TNLs) to transcriptionally mobilise resistance pathways. By interrogating the Arabidopsis EDS1 ɑ-helical EP-domain we identify positively charged residues lining a cavity that are essential for TNL immunity signalling, beyond heterodimer formation. Mutating a single, conserved surface arginine (R493) disables TNL immunity to an oomycete pathogen and to bacteria producing the virulence factor, coronatine. Plants expressing a weakly active EDS1(R493A) variant have delayed transcriptional reprogramming, with severe consequences for resistance and countering bacterial coronatine repression of early immunity genes. The same EP-domain surface is utilised by a non-TNL receptor RPS2 for bacterial immunity, indicating that the EDS1 EP-domain signals in resistance conferred by different NLR receptor types. These data provide a unique structural insight to early downstream signalling in NLR receptor immunity.
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spelling pubmed-63776072019-02-19 An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis Bhandari, Deepak D. Lapin, Dmitry Kracher, Barbara von Born, Patrick Bautor, Jaqueline Niefind, Karsten Parker, Jane E. Nat Commun Article Plant intracellular NLR receptors recognise pathogen interference to trigger immunity but how NLRs signal is not known. Enhanced disease susceptibility1 (EDS1) heterodimers are recruited by Toll-interleukin1-receptor domain NLRs (TNLs) to transcriptionally mobilise resistance pathways. By interrogating the Arabidopsis EDS1 ɑ-helical EP-domain we identify positively charged residues lining a cavity that are essential for TNL immunity signalling, beyond heterodimer formation. Mutating a single, conserved surface arginine (R493) disables TNL immunity to an oomycete pathogen and to bacteria producing the virulence factor, coronatine. Plants expressing a weakly active EDS1(R493A) variant have delayed transcriptional reprogramming, with severe consequences for resistance and countering bacterial coronatine repression of early immunity genes. The same EP-domain surface is utilised by a non-TNL receptor RPS2 for bacterial immunity, indicating that the EDS1 EP-domain signals in resistance conferred by different NLR receptor types. These data provide a unique structural insight to early downstream signalling in NLR receptor immunity. Nature Publishing Group UK 2019-02-15 /pmc/articles/PMC6377607/ /pubmed/30770836 http://dx.doi.org/10.1038/s41467-019-08783-0 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Bhandari, Deepak D.
Lapin, Dmitry
Kracher, Barbara
von Born, Patrick
Bautor, Jaqueline
Niefind, Karsten
Parker, Jane E.
An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis
title An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis
title_full An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis
title_fullStr An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis
title_full_unstemmed An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis
title_short An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis
title_sort eds1 heterodimer signalling surface enforces timely reprogramming of immunity genes in arabidopsis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6377607/
https://www.ncbi.nlm.nih.gov/pubmed/30770836
http://dx.doi.org/10.1038/s41467-019-08783-0
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