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CELL BIOLOGY AND SIGNAL TRANSDUCTION

BWMK1, a Rice Mitogen-Activated Protein Kinase, Locates in the Nucleus and Mediates Pathogenesis-Related Gene Expression by Activation of a Transcription Factor¹

Division of Applied Life Science (BK21 Program) and Plant Molecular Biology and Biotechnology Research Center, Gyeongsang National University, Jinju 660–701, Korea

Mitogen-activated protein kinase (MAPK) cascades are known to transduce plant defense signals, but the downstream components of the MAPK have as yet not been elucidated. Here, we report an MAPK from rice (Oryza sativa), BWMK1, and a transcription factor, OsEREBP1, phosphorylated by the kinase. The MAPK carries a TDY phosphorylation motif instead of the more common TEY motif in its kinase domain and has an unusually extended C-terminal domain that is essential to its kinase activity and translocation to the nucleus. The MAPK phosphorylates OsEREBP1 that binds to the GCC box element (AGCCGCC) of the several basic pathogenesis-related gene promoters, which in turn enhances DNA-binding activity of the factor to the cis element in vitro. Transient co-expression of the BWMK1 and OsEREBP1 in Arabidopsis protoplasts elevates the expression of the -glucuronidase reporter gene driven by the GCC box element. Furthermore, transgenic tobacco (Nicotiana tabacum) plants overexpressing BWMK1 expressed many pathogenesis-related genes at higher levels than wild-type plants with an enhanced resistance to pathogens. These findings suggest that MAPKs contribute to plant defense signal transduction by phosphorylating one or more transcription factors.

¹ This work was supported by Korea Science and Engineering Foundation (grant no. 2000–2–20900–001–1), by Crop Functional Genomic Center (grant no. CG1512), by National Research Laboratory (grant no. 2000–N–NL–01–C–236), and by the BK21 program from the Ministry of Education to M.J.C.

² These authors contributed equally to the paper.

^* Corresponding author; e-mail mjcho{at}nongae.gsnu.ac.kr; fax 82–55–759–9363.

Received March 6, 2003; returned for revision April 7, 2003; accepted May 9, 2003.

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