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PNAS 107 (17): 8029-8034

Copyright © 2010 by the National Academy of Sciences.


An ATPase promotes autophosphorylation of the pattern recognition receptor XA21 and inhibits XA21-mediated immunity

Xuewei Chen, Mawsheng Chern, Patrick E. Canlas, Deling Ruan, Caiying Jiang1, and Pamela C. Ronald2

Department of Plant Pathology, University of California, Davis, CA 95616

Edited by David C. Baulcombe, University of Cambridge, Cambridge, United Kingdom, and approved March 18, 2010 (received for review October 24, 2009)

Abstract: Cell-surface pattern recognition receptors (PRRs) are key components of the innate immune response in animals and plants. These receptors typically carry or associate with non-RD kinases to control early events of innate immunity signaling. Despite their importance, the mode of regulation of PRRs is largely unknown. Here we show that the rice PRR, XA21, interacts with XA21 binding protein 24 (XB24), a previously undescribed ATPase. XB24 promotes autophosphorylation of XA21 through its ATPase activity. Rice lines silenced for Xb24 display enhanced XA21-mediated immunity, whereas rice lines overexpressing XB24 are compromised for immunity. XB24 ATPase enzyme activity is required for XB24 function. XA21 is degraded in the presence of the pathogen-associated molecular pattern Ax21 when XB24 is overexpressed. These results demonstrate a function for this large class of broadly conserved ATPases in PRR-mediated immunity.

Key Words: non-RD kinase • pathogen-associated molecular pattern • pattern recognition receptor • ATPase • rice

Freely available online through the PNAS open access option.

Author contributions: X.C. and P.C.R. designed research; X.C., P.E.C., D.R., and C.J. performed research; X.C., M.C., and P.C.R. analyzed data; and X.C., M.C., and P.C.R. wrote the paper.

1Present address: College of Life Science, Zhejiang Sci-Tech University, Hangzhou 310018, China.

The authors declare no conflict of interest.

This article is a PNAS Direct Submission.

This article contains supporting information online at

2To whom correspondence should be addressed. E-mail: pcronald{at}

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