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Published on May 8, 2003; 10.1104/pp.102.019802


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Received December 26, 2002
Returned for revision January 27, 2003
Accepted March 20, 2003

Transcriptome Profiling of Sulfur-Responsive Genes in Arabidopsis Reveals Global Effects of Sulfur Nutrition on Multiple Metabolic Pathways1[w]

Akiko Maruyama-Nakashita , Eri Inoue , Akiko Watanabe-Takahashi , Tomoyuki Yamaya , and Hideki Takahashi *

RIKEN Plant Science Center, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama 230-0045, Japan (A.M.-N., E.I., A.W.-T., T.Y., H.T.); and Tohoku University, Graduate School of Agricultural Sciences, 1-1 Tsutsumidori-Amamiyamachi, Aoba-ku, Sendai 981-8555, Japan (T.Y.)

* Corresponding author; email: hideki{at}postman.riken.go.jp.

Sulfate is a macronutrient required for cell growth and development. Arabidopsis has two high-affinity sulfate transporters (SULTR1;1 and SULTR1;2) that represent the sulfate uptake activities at the root surface. Sulfur limitation (-S) response relevant to the function of SULTR1;2 was elucidated in this study. We have isolated a novel T-DNA insertion allele defective in the SULTR1;2 sulfate transporter. This mutant, sel1-10, is allelic with the sel1 mutants identified previously in a screen for increased tolerance to selenate, a toxic analog of sulfate (Shibagaki et al., 2002). The abundance of SULTR1;1 mRNA was significantly increased in the sel1-10 mutant; however, this compensatory up-regulation of SULTR1;1 was not sufficient to restore the growth. The sulfate content of the mutant was 10% to 20% of the wild type, suggesting that induction of SULTR1;1 is not fully complementing the function of SULTR1;2 and that SULTR1;2 serves as the major facilitator for the acquisition of sulfate in Arabidopsis roots. Transcriptome analysis of approximately 8,000 Arabidopsis genes in the sel1-10 mutant suggested that dysfunction of the SULTR1;2 transporter can mimic general -S symptoms. Hierarchal clustering of sulfur responsive genes in the wild type and mutant indicated that sulfate uptake, reductive sulfur assimilation, and turnover of secondary sulfur metabolites are activated under -S. The profiles of -S-responsive genes further suggested induction of genes that may alleviate oxidative damage and generation of reactive oxygen species caused by shortage of glutathione.




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