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Plant and Cell Physiology Advance Access originally published online on July 2, 2006
Plant and Cell Physiology 2006 47(8):1035-1044; doi:10.1093/pcp/pcj074
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© The Author 2006. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Regulatory Mechanisms of ROI Generation are Affected by Rice spl Mutations

Kaori Kojo1, Takashi Yaeno1, Kensuke Kusumi1, Hideo Matsumura2, Shizuko Fujisawa2, Ryohei Terauchi2 and Koh Iba1,*

1 Department of Biology, Faculty of Sciences, Kyushu University, Hakozaki, Fukuoka, 812-8581 Japan
2 Iwate Biotechnology Research Center, Narita 22-174-4, Kitakami, Iwate, 024-0003 Japan

* Corresponding author: E-mail, koibascb{at}mbox.nc.kyushu-u.ac.jp; Fax, +81-92-642-2621.

Reactive oxygen intermediates (ROIs) play a pivotal role in the hypersensitive response (HR) in disease resistance. NADPH oxidase is a major source of ROI; however, the mechanisms of its regulation are unclear. Rice spl mutants spontaneously form lesions which resemble those occurring during the HR, suggesting that the mutations affect regulation of the HR. We found that spl2, spl7 and spl11 mutant cells accumulated increased amounts of H2O2 in response to rice blast fungal elicitor. Increased accumulation of ROIs was suppressed by inhibition of NADPH oxidase in the spl cells, and was also observed in the ozone-exposed spl plants. These mutants have sufficient activities of ROI-scavenging enzymes compared with the wild type. In addition, spl7 mutant cells accumulated higher amounts of H2O2 when treated with calyculin A (CA), an inhibitor of protein phosphatase. Furthermore, spl2 mutant plants exhibited accelerated accumulation of H2O2 and increased rates of cell death in response to wounding. These results suggest that the spl2, spl7 and spl11 mutants are defective in the regulation of NADPH oxidase, and the spl7 mutation may give rise to enhancement of the signaling pathway which protein dephosphorylation controls, while the spl2 mutation affects both the pathogen-induced and wound-induced signaling pathways.

(Received May 23, 2006; Accepted June 2, 2006)
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