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

Deepak D. Bhandari; Dmitry Lapin; Barbara Kracher; Patrick von Born; Jaqueline Bautor; Karsten Niefind; Jane E. Parker

doi:10.1038/s41467-019-08783-0

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

Deepak D. Bhandari, Dmitry Lapin, Barbara Kracher, Patrick von Born, Jaqueline Bautor, Karsten Niefind, Jane E. Parker^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

Abstract

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.

Original language	English
Article number	772
Journal	Nature Communications
Volume	10
Issue number	1
DOIs	https://doi.org/10.1038/s41467-019-08783-0
Publication status	Published - 1 Dec 2019
Externally published	Yes

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title = "An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis",

abstract = " 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. ",

author = "Bhandari, {Deepak D.} and Dmitry Lapin and Barbara Kracher and {von Born}, Patrick and Jaqueline Bautor and Karsten Niefind and Parker, {Jane E.}",

note = "Funding Information: We thank Kenichi Tsuda and Takaki Maekawa (MPIPZ Cologne) for helpful discussions. This work was supported by The Max-Planck Society and Deutsche For-schungsgemeinschaft (DFG) grants within SFB 635 and SFB 670 (JEP, DDB), SFB 680 (JEP, DL), and an International Max-Planck Research School (IMPRS) doctoral fellowship (PvB). Publisher Copyright: {\textcopyright} 2019, The Author(s).",

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AU - Niefind, Karsten

AU - Parker, Jane E.

N1 - Funding Information: We thank Kenichi Tsuda and Takaki Maekawa (MPIPZ Cologne) for helpful discussions. This work was supported by The Max-Planck Society and Deutsche For-schungsgemeinschaft (DFG) grants within SFB 635 and SFB 670 (JEP, DDB), SFB 680 (JEP, DL), and an International Max-Planck Research School (IMPRS) doctoral fellowship (PvB). Publisher Copyright: © 2019, The Author(s).

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N2 - 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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An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis

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