Brassinosteroids inhibit pathogen-associated molecular pattern–triggered immune signaling independent of the receptor kinase BAK1.

C. Albrecht, F. Boutrot, C. Segonzac, B. Schwessinger, S. Gimenez-Ibanez, J.P. Rathjen, D. Chinchilla, S.C. de Vries, C. Zipfel

Research output: Contribution to journalArticleAcademicpeer-review

226 Citations (Scopus)

Abstract

Plants and animals use innate immunity as a first defense against pathogens, a costly yet necessary tradeoff between growth and immunity. In Arabidopsis, the regulatory leucine-rich repeat receptor-like kinase (LRR-RLK) BAK1 combines with the LRR-RLKs FLS2 and EFR in pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and the LRR-RLK BRI1 in brassinosteroid (BR)-mediated growth. Therefore, a potential tradeoff between these pathways mediated by BAK1 is often postulated. Here, we show a unidirectional inhibition of FLS2-mediated immune signaling by BR perception. Unexpectedly, this effect occurred downstream or independently of complex formation with BAK1 and associated downstream phosphorylation. Thus, BAK1 is not rate-limiting in these pathways. BRs also inhibited signaling triggered by the BAK1-independent recognition of the fungal PAMP chitin. Our results suggest a general mechanism operative in plants in which BR-mediated growth directly antagonizes innate immune signaling.
Original languageEnglish
Pages (from-to)303-308
JournalProceedings of the National Academy of Sciences of the United States of America
Volume109
Issue number1
DOIs
Publication statusPublished - 2012

Keywords

  • plant innate immunity
  • disease resistance
  • gene-expression
  • protein complex
  • arabidopsis
  • growth
  • pathways
  • fls2
  • responses
  • acid

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