Arabidopsis SLIM1 is a central transcriptional regulator of plant sulfur response and metabolism

被引:278
作者
Maruyama-Nakashita, Akiko
Nakamura, Yumiko
Tohge, Takayuki
Saito, Kazuki
Takahashi, Hideki [1 ]
机构
[1] RIKEN, Plant Sci Ctr, Tsurumi Ku, Yokohama, Kanagawa 2300045, Japan
[2] Chiba Univ, Grad Sch Pharmaceut Sci, Inage Ku, Chiba 2638522, Japan
关键词
AFFINITY SULFATE TRANSPORTERS; GLUCOSINOLATE BIOSYNTHESIS; NUCLEAR-PROTEIN; ETHYLENE GAS; GENE-FAMILY; EXPRESSION; THALIANA; PATHWAY; ASSIMILATION; ROOTS;
D O I
10.1105/tpc.106.046458
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:3235 / 3251
页数:17
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