Plant Physiology Preview
Published on January 11, 2006; 10.1104/pp.105.074906
Received November 30, 2005
Returned for revision December 16, 2005
Accepted December 16, 2005
Rewiring Mitogen-Activated Protein Kinase Cascade by Positive Feedback Confers Potato Blight Resistance
Chihiro Yamamizo , Kazuo Kuchimura , Akira Kobayashi , Shinpei Katou , Kazuhito Kawakita , Jonathan D. G. Jones , Noriyuki Doke , and Hirofumi Yoshioka *
Graduate school of Bioagricultural Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan
Department of Upland Agriculture, National Agricultural Research Center of Hokkaido Region, Memuro, Hokkaido 082-0071, Japan
Sainsbury Laboratory, John Innes Centre, Colney Lane, Norwich NR4 7UH, United Kingdom
* Corresponding author; email: hyoshiok{at}agr.nagoya-u.ac.jp.
Late blight, caused by the notorious pathogen Phytophthora infestans, is a devastating disease of potato (Solanum tuberosum) and tomato (Lycopersicon esculentum), and during 1840s caused the Irish potato famine and over one million fatalities. Currently grown potato cultivars lack adequate blight tolerance. Earlier cultivars bred for resistance used disease resistance (R) genes that confer immunity only to some strains of the pathogen harboring corresponding avirulence (Avr) gene. Specific R-mediated immunity and chemical controls are rapidly overcome in the field when new pathogen races arise through mutation, recombination or migration from elsewhere. A mitogen-activated protein kinase (MAPK) cascade plays a pivotal role in plant innate immunity. Here we show that the transgenic potato plants that carry a constitutively active form of MAPK kinase (MAPKK) driven by a pathogen-inducible promoter of potato, showed high resistance to early blight pathogen Alternaria solani as well as P. infestans. The pathogen attack provoked defense-related MAPKs activation followed by induction of NADPH oxidase gene expression, which is implicated in reactive oxygen species production, and resulted in hypersensitive response (HR)-like phenotype. We propose that enhancing disease resistance through altered regulation of plant defense mechanisms should be more durable and publicly acceptable than engineering overexpression of antimicrobial proteins.
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