Enhanced disease susceptibility 1 and salicylic acid act redundantly to regulate resistance gene-mediated signaling

Srivathsa C. Venugopal, Rae Dong Jeong, Mihir K. Mandal, Shifeng Zhu, A. C. Chandra-Shekara, Ye Xia, Matthew Hersh, Arnold J. Stromberg, Du Roy Navarre, Aardra Kachroo, Pradeep Kachroo

Research output: Contribution to journalArticlepeer-review

128 Scopus citations

Abstract

Resistance (R) protein-associated pathways are well known to participate in defense against a variety of microbial pathogens. Salicylic acid (SA) and its associated proteinaceous signaling components, including enhanced disease susceptibility 1 (EDS1), non-race-specific disease resistance 1 (NDR1), phytoalexin deficient 4 (PAD4), senescence associated gene 101 (SAG101), and EDS5, have been identified as components of resistance derived from many R proteins. Here, we show that EDS1 and SA fulfill redundant functions in defense signaling mediated by R proteins, which were thought to function independent of EDS1 and/or SA. Simultaneous mutations in EDS1 and the SA-synthesizing enzyme SID2 compromised hypersensitive response and/or resistance mediated by R proteins that contain coiled coil domains at their Nterminal ends. Furthermore, the expression of R genes and the associated defense signaling induced in response to a reduction in the level of oleic acid were also suppressed by compromising SA biosynthesis in the eds1 mutant background. The functional redundancy with SA was specific to EDS1. Results presented here redefine our understanding of the roles of EDS1 and SA in plant defense.

Original languageEnglish
Article numbere1000545
JournalPLoS Genetics
Volume5
Issue number7
DOIs
StatePublished - Jul 2009

ASJC Scopus subject areas

  • Ecology, Evolution, Behavior and Systematics
  • Molecular Biology
  • Genetics
  • Genetics(clinical)
  • Cancer Research

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