First published online November 17, 2006; 10.1105/tpc.106.046458
The Plant Cell 18:3235-3251 (2006)
© 2006 American Society of Plant Biologists
OPEN ACCESS ARTICLE
Arabidopsis SLIM1 Is a Central Transcriptional Regulator of Plant Sulfur Response and Metabolism[W],[OA]
Akiko Maruyama-Nakashitaa,
Yumiko Nakamuraa,
Takayuki Tohgea,
Kazuki Saitoa,b and
Hideki Takahashia,1
a RIKEN Plant Science Center, Tsurumi-ku, Yokohama 230-0045, Japan
b Graduate School of Pharmaceutical Sciences, Chiba University, Inage-ku, Chiba 263-8522, Japan
1 To whom correspondence should be addressed. E-mail hideki{at}riken.jp; fax 81-45-503-9650.
Sulfur is an essential macronutrient required for plant growth. To identify key transcription factors regulating the sulfur assimilatory pathway, we screened Arabidopsis thaliana mutants using a fluorescent reporter gene construct consisting of the sulfur limitation-responsive promoter of the SULTR1;2 sulfate transporter and green fluorescent protein as a background indicator for monitoring plant sulfur responses. The isolated mutant, sulfur limitation1 (slim1), was unable to induce SULTR1;2 transcripts under low-sulfur (S) conditions. Mutations causing the sulfur limitation responseless phenotypes of slim1 were identified in an EIL family transcription factor, ETHYLENE-INSENSITIVE3-LIKE3 (EIL3), whose functional identity with SLIM1 was confirmed by genetic complementation. Sulfate uptake and plant growth on S were significantly reduced by slim1 mutations but recovered by overexpression of SLIM1. SLIM1 functioned as a central transcriptional regulator, which controlled both the activation of sulfate acquisition and degradation of glucosinolates under S conditions. Metabolite analysis indicated stable accumulation of glucosinolates in slim1 mutants, even under S conditions, particularly in the molecular species with methylsulfinylalkyl side chains beneficial to human health. Overexpression of SLIM1 and its rice (Oryza sativa) homologs, but no other EIL genes of Arabidopsis, restored the sulfur limitation responseless phenotypes of slim1 mutants, suggesting uniqueness of the SLIM1/EIL3 subgroup members as sulfur response regulators.
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