Yamaguchi Chisato, Khamsalath Soudthedlath, Takimoto Yuki, Suyama Akiko, Mori Yuki, Ohkama-Ohtsu Naoko, Maruyama-Nakashita Akiko
Department of Bioscience and Biotechnology, Graduate School of Bioresource and Bioenvironmental Sciences, Faculty of Agriculture, Kyushu University, 744 Motooka, Nishi-ku, Fukuoka 819-0395, Japan.
NARO Tohoku Agricultural Research Center, 4 Akahira, Shimo-Kuriyagawa, Morioka 020-0198, Japan.
Plants (Basel). 2020 Jan 29;9(2):163. doi: 10.3390/plants9020163.
Sulfur (S) assimilation, which is initiated by sulfate uptake, generates cysteine, the substrate for glutathione (GSH) and phytochelatin (PC) synthesis. GSH and PC contribute to cadmium (Cd) detoxification by capturing it for sequestration. Although Cd exposure is known to induce the expression of S-assimilating enzyme genes, including sulfate transporters (SULTRs), mechanisms of their transcriptional regulation are not well understood. Transcription factor SLIM1 controls transcriptional changes during S deficiency (-S) in Arabidopsis thaliana. We examined the potential involvement of SLIM1 in inducing the S assimilation pathway and PC accumulation. Cd treatment reduced the shoot fresh weight in the sulfur limitation1 (slim1) mutant but not in the parental line (1;2PGN). Cd-induced increases of sulfate uptake and SULTR1;2 expressions were diminished in the slim1 mutant, suggesting that SLIM1 is involved in inducing sulfate uptake during Cd exposure. The GSH and PC levels were lower in slim1 than in the parental line, indicating that SLIM1 was required for increasing PC during Cd treatment. Hence, SLIM1 indirectly contributes to Cd tolerance of plants by inducing -S responses in the cell caused by depleting the GSH pool, which is consumed by enhanced PC synthesis and sequestration to the vacuole.
硫（S）同化作用由硫酸盐吸收引发，可生成半胱氨酸，而半胱氨酸是谷胱甘肽（GSH）和植物螯合肽（PC）合成的底物。GSH和PC通过捕获镉（Cd）进行螯合，从而有助于镉的解毒。虽然已知镉暴露会诱导包括硫酸盐转运蛋白（SULTRs）在内的硫同化酶基因的表达，但其转录调控机制尚不清楚。转录因子SLIM1控制拟南芥在缺硫（-S）期间的转录变化。我们研究了SLIM1在诱导硫同化途径和PC积累方面的潜在作用。镉处理降低了硫限制1（slim1）突变体地上部的鲜重，但在亲本系（1;2PGN）中未出现这种情况。镉诱导的硫酸盐吸收增加和SULTR1;2表达在slim1突变体中减弱，这表明SLIM1参与了镉暴露期间的硫酸盐吸收诱导过程。slim1中的GSH和PC水平低于亲本系，这表明在镉处理期间增加PC需要SLIM1。因此，SLIM1通过诱导细胞中的-S反应间接有助于植物对镉的耐受性，这种反应是由谷胱甘肽池耗尽引起的，谷胱甘肽池因PC合成增强和向液泡的螯合而被消耗。
