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

Deepak D. Bhandari, Dmitry Lapin, Barbara Kracher, Patrick Born, Jaqueline Bautor, Karsten Niefind and Jane E. Parker ()
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Deepak D. Bhandari: Max-Planck Institute for Plant Breeding Research
Dmitry Lapin: Max-Planck Institute for Plant Breeding Research
Barbara Kracher: Max-Planck Institute for Plant Breeding Research
Patrick Born: Max-Planck Institute for Plant Breeding Research
Jaqueline Bautor: Max-Planck Institute for Plant Breeding Research
Karsten Niefind: University of Cologne
Jane E. Parker: Max-Planck Institute for Plant Breeding Research

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: 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 EDS1R493A 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.

Date: 2019
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DOI: 10.1038/s41467-019-08783-0

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