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PNAS 109 (1): 303-308

Copyright © 2012 by the National Academy of Sciences.


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

Catherine Albrechta,1, Freddy Boutrotb,1, Cécile Segonzacb, Benjamin Schwessingerb,2, Selena Gimenez-Ibanezb,3, Delphine Chinchillac, John P. Rathjenb,4, Sacco C. de Vriesa, and Cyril Zipfelb,5

aLaboratory of Biochemistry, Wageningen University, 6703 HA Wageningen, The Netherlands; bThe Sainsbury Laboratory, Norwich Research Park, Norwich NR4 7UH, United Kingdom; and cZurich-Basel Plant Science Center, Botanical Institute, University of Basel, 4056 Basel, Switzerland

Edited* by June B. Nasrallah, Cornell University, Ithaca, NY, and approved October 20, 2011 (received for review June 21, 2011)

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.

Key Words: flagellin sensing 2 • brassinosteroid insensitive 1 • BRI1-associated kinase 1 • cross-talk

Author contributions: C.A., F.B., C.S., B.S., S.G.-I., D.C., J.P.R., S.C.d.V., and C.Z. designed research; C.A., F.B., C.S., B.S., and S.G.-I. performed research; C.A., F.B., C.S., B.S., S.G.-I., D.C., J.P.R., S.C.d.V., and C.Z. analyzed data; and C.A., F.B., S.C.d.V., and C.Z. wrote the paper.

1C.A. and F.B. contributed equally to this work.

2Present address: Department of Plant Pathology, College of Agricultural and Environmental Sciences, University of California, Davis, CA 95616.

3Present address: Centro Nacional de Biotecnologia, 28049 Madrid, Spain.

4Present address: Research School of Biology, Australian National University, Canberra 0200, Australia.

The authors declare no conflict of interest.

*This Direct Submission article had a prearranged editor.

See Commentary on page 7.

This article contains supporting information online at

5To whom correspondence should be addressed. E-mail: cyril.zipfel{at}

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