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PNAS 109 (1): 297-302

Copyright © 2012 by the National Academy of Sciences.


Brassinosteroids modulate the efficiency of plant immune responses to microbe-associated molecular patterns

Youssef Belkhadira,b,1, Yvon Jaillaisa,b,1, Petra Epplec, Emilia Balsemão-Piresa,b,2, Jeffery L. Danglc,d,3, and Joanne Chorya,b,3

aPlant Biology Laboratory and bHoward Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037; and cHoward Hughes Medical Institute, Department of Biology, and dDepartment of Microbiology and Immunology, Curriculum in Genetics, Carolina Center for Genome Sciences, University of North Carolina, Chapel Hill, NC 27599

Contributed by Joanne Chory, August 6, 2011 (sent for review June 16, 2011)

Abstract: Metazoans and plants use pattern recognition receptors (PRRs) to sense conserved microbial-associated molecular patterns (MAMPs) in the extracellular environment. In plants, the bacterial MAMPs flagellin and elongation factor Tu (EF-Tu) activate distinct, phylogenetically related cell surface pattern recognition receptors of the leucine-rich repeat receptor kinase (LRR-RK) family called FLS2 and EF-Tu receptor, respectively. BAK1 is an LRR-RK coreceptor for both FLS2 and EF-Tu receptor. BAK1 is also a coreceptor for the plant brassinosteroid (BR) receptor, the LRR-RK BRI1. Binding of BR to BRI1 primarily promotes cell elongation. Here, we tune the BR pathway response to establish how plant cells can generate functionally different cellular outputs in response to MAMPs and pathogens. We demonstrate that BR can act antagonistically or synergistically with responses to MAMPs. We further show that the synergistic activities of BRs on MAMP responses require BAK1. Our results highlight the importance of plant steroid homeostasis as a critical step in the establishment of plant immunity. We propose that tradeoffs associated with plasticity in the face of infection are layered atop plant steroid developmental programs.

Key Words: brassinosteroid signaling • plant immune system signaling • signaling crosstalk

Author contributions: Y.B., Y.J., P.E., E.B.-P., J.L.D., and J.C. designed research; Y.B., Y.J., P.E., and E.B.-P. performed research; Y.B., Y.J., P.E., E.B.-P., J.L.D., and J.C. analyzed data; and Y.B., Y.J., P.E., J.L.D., and J.C. wrote the paper.

1Y.B. and Y.J. contributed equally to this work.

2Present address: Department of Genetics, Laboratório de Genômica Funcional e Transdução de Sinal, Universidade Federal do Rio de Janeiro, 21944-970, Rio de Janeiro, Brazil.

The authors declare no conflict of interest.

See Commentary on page 7.

This article contains supporting information online at

3To whom correspondence may be addressed. E-mail: chory{at} or dangl{at}

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