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The receptor-like kinase SERK3/BAK1 is a central regulator of innate immunity in plants
Antje Heese*,,
Dagmar R. Hann,
Selena Gimenez-Ibanez,
Alexandra M. E. Jones,
Kai He,
Jia Li,
Julian I. Schroeder¶,
Scott C. Peck,||, and
John P. Rathjen,
*Department of Biochemistry, University of Missouri, 540G Bond Life Sciences Center,1201 Rollins Road, Columbia, MO 65211; The Sainsbury Laboratory, Norwich Research Park, Colney Norwich NR4 7UH, United Kingdom; Department of Botany and Microbiology, University of Oklahoma, Norman, OK 73019; and ¶Division of Biological Sciences, Cell and Developmental Biology, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0346
Communicated by David Baulcombe, The Sainsbury Laboratory, Norwich, United Kingdom, June 6, 2007
Received for publication May 25, 2007.
Abstract:
In pathogen-associated molecular pattern (PAMP)-triggered immunity(PTI), plant cell surface receptors sense potential microbialpathogens by recognizing elicitors called PAMPs. Although diversePAMPs trigger PTI through distinct receptors, the resultingintracellular responses overlap extensively. Despite this, acommon component(s) linking signal perception with transductionremains unknown. In this study, we identify SOMATIC EMBRYOGENESISRECEPTOR KINASE (SERK)3/brassinosteroid-associated kinase (BAK)1,a receptor-like kinase previously implicated in hormone signaling,as a component of plant PTI. In Arabidopsis thaliana, AtSERK3/BAK1rapidly enters an elicitor-dependent complex with FLAGELLINSENSING 2 (FLS2), the receptor for the bacterial PAMP flagellinand its peptide derivative flg22. In the absence of AtSERK3/BAK1,early flg22-dependent responses are greatly reduced in bothA. thaliana and Nicotiana benthamiana. Furthermore, N. benthamianaSerk3/Bak1 is required for full responses to unrelated PAMPsand, importantly, for restriction of bacterial and oomyceteinfections. Thus, SERK3/BAK1 appears to integrate diverse perceptionevents into downstream PAMP responses, leading to immunity againsta range of invading microbes.
Author contributions: A.H. and D.R.H. contributed equally tothis work; A.H., D.R.H., and J.P.R. designed research; A.H.,D.R.H., S.G.-I., and A.M.E.J. performed research; A.H., D.R.H.,S.G.-I., K.H., J.L., J.I.S., S.C.P., and J.P.R. contributednew reagents/analytic tools; A.H., D.R.H., S.G.-I., A.M.E.J.,S.C.P., and J.P.R. analyzed data; and A.H., D.R.H., and J.P.R.wrote the paper.
||Present address: Department of Biochemistry, University ofMissouri, 271H Bond Life Sciences Center, 1201 Rollins Road,Columbia, MO 65211.
The authors declare no conflict of interest.
Data deposition: The sequences reported in this paper have beendeposited in the GenBank database [accession nos. CK291393 (NbSerk3)and CK291392 (NbSerk2)].
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