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

SUBMITTER: Bhandari DD 

PROVIDER: S-EPMC6377607 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature