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- Title
An EDS1 heterodimer signalling surface enforces timely reprogramming of immunity genes in Arabidopsis.
- Authors
Bhandari, Deepak D.; Lapin, Dmitry; Kracher, Barbara; von Born, Patrick; Bautor, Jaqueline; Niefind, Karsten; Parker, Jane E.
- 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. CC and TIR-domain type NLR receptors trigger plant immunity in response to pathogen effectors. Here, Bhandari et al. show that the EP-domain surface of EDS1 heterodimers signals downstream of both receptor types and ensures a rapid transcriptional response in TIR-NLR immunity to bacteria.
- Publication
Nature Communications, 2019, Vol 10, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-019-08783-0