Glucose enhances indolic glucosinolate biosynthesis without reducing primary sulfur assimilation.
Glucose enhances indolic glucosinolate biosynthesis without reducing primary sulfur assimilation.
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葡萄糖增强吲哚芥子油苷的生物合成而不减少初级硫同化
DOI：
10.1038/srep31854
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发表时间：
2016-08-23
影响因子：
4.6
通讯作者：
Wang Q
中科院分区：
文献类型：
--
作者：
Miao H;Cai C;Wei J;Huang J;Chang J;Qian H;Zhang X;Zhao Y;Sun B;Wang B;Wang Q
葡萄糖作为信号分子对硫代葡萄糖苷生物合成的诱导作用在我们以前的研究中已有报道。本文进一步研究了葡萄糖对拟南芥吲哚硫苷生物合成的调控机制。葡萄糖对吲哚硫代葡萄糖苷的生物合成产生积极影响，表现为葡萄糖处理诱导吲哚硫代葡萄糖苷的积累和相关基因的表达增强。遗传分析表明，MYB 34和MYB 51在维持基础吲哚芥子油苷积累中至关重要，其中MYB 34在响应葡萄糖信号传导中起关键作用。在thegin 2 - 1突变体中，葡萄糖引起的吲哚芥子油苷积累增加和MYB 34、MYB 51和MYB 122的mRNA水平降低，表明HXK 1在葡萄糖介导的吲哚芥子油苷生物合成中起重要作用。与已知的ABI 5在葡萄糖介导的脂肪族硫代葡萄糖苷生物合成中的功能相反，葡萄糖诱导的吲哚硫代葡萄糖苷积累不需要ABI 5。此外，我们的研究结果还表明，葡萄糖诱导的硫代葡萄糖苷积累是由于硫同化作用的增强，而不是直接硫分配到硫代葡萄糖苷的生物合成。因此，我们的数据提供了新的见解葡萄糖调节硫代葡萄糖苷生物合成的分子机制。
The effect of glucose as a signaling molecule on induction of aliphatic glucosinolate biosynthesis was reported in our former study. Here, we further investigated the regulatory mechanism of indolic glucosinolate biosynthesis by glucose inArabidopsis. Glucose exerted a positive influence on indolic glucosinolate biosynthesis, which was demonstrated by induced accumulation of indolic glucosinolates and enhanced expression of related genes upon glucose treatment. Genetic analysis revealed that MYB34 and MYB51 were crucial in maintaining the basal indolic glucosinolate accumulation, with MYB34 being pivotal in response to glucose signaling. The increased accumulation of indolic glucosinolates and mRNA levels ofMYB34,MYB51andMYB122caused by glucose were inhibited in thegin2-1mutant, suggesting an important role of HXK1 in glucose-mediated induction of indolic glucosinolate biosynthesis. In contrast to what was known on the function of ABI5 in glucose-mediated aliphatic glucosinolate biosynthesis, ABI5 was not required for glucose-induced indolic glucosinolate accumulation. In addition, our results also indicated that glucose-induced glucosinolate accumulation was due to enhanced sulfur assimilation instead of directed sulfur partitioning into glucosinolate biosynthesis. Thus, our data provide new insights into molecular mechanisms underlying glucose-regulated glucosinolate biosynthesis.