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Plant Physiology Preview Published on March 25, 2009; 10.1104/pp.108.134700
OPEN ACCESS ARTICLE
Received January 5, 2009 STOP1 (Sensitive TO Proton Rhizotoxicity 1) Regulates Multiple Genes which Protect Arabidopsis from Proton and Aluminum Toxicities
Laboratory of Plant Cell Technology, Faculty of Applied Biological Sciences, Gifu University, Gifu, Gifu, 501-1193, Japan; Experimental Plant Division, RIKEN-BRC, Tsukuba, Ibaraki 305-0074, Japan; Laboratory of Genome Biotechnology, Kazusa DNA Research Institute, Kisarazu, Chiba 292–0818, Japan; RIKEN Plant Science Center, Tsurumi-ku, Yokohama 230-0045, Japan * Corresponding author; email: koyama{at}gifu-u.ac.jp.
The Arabidopsis mutant stop1 (sensitive to proton rhizotoxicity 1) carries a missense mutation at an essential domain of the His2-Cys2 zinc finger protein STOP1. Transcriptome analyses revealed that various genes were down-regulated in the mutant, indicating that STOP1 is involved in signal transduction pathways regulating aluminum (Al) and H+ responsive gene expression. The Al-hypersensitivity of the mutant could be caused by down-regulation of AtALMT1 (Arabidopsis Al-activated malate transporter gene) and ALS3 (aluminum sensitive 3). This hypothesis was supported by comparison of Al tolerance among T-DNA insertion lines and a transgenic stop-mutant carrying 35S::AtALMT1. All T-DNA insertion lines of STOP1, AtALMT1 and ALS3 were sensitive to Al, but introduction of CaMV35S::AtALMT1 did not completely recover Al tolerance of the stop1-mutant. Down-regulation of various genes involved in ion homeostasis and pH regulating metabolism in the mutant were also identified by microarray analyses. CIPK23 (CBL-interacting protein kinase 23) regulating major K+ transporter and a sulfate transporter SULT3;5 were down-regulated in the mutant. In addition, integral profiling of the metabolites and transcripts revealed that pH regulating metabolisms such as the GABA (
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