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首页> 外文期刊>Journal of Experimental Botany >Overexpression of HMG-CoA synthase promotes Arabidopsis root growth and adversely affects glucosinolate biosynthesis
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Overexpression of HMG-CoA synthase promotes Arabidopsis root growth and adversely affects glucosinolate biosynthesis

机译：HMG-CoA合酶的过度表达促进拟南芥根系生长，并且不利地影响葡糖苷生物合成

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3-Hydroxy-3-methylglutaryl-CoA synthase (HMGS) catalyses the second step of the mevalonate (MVA) pathway. An HMGS inhibitor (F-244) has been reported to retard growth in wheat, tobacco, and Brassica juncea, but the mechanism remains unknown. Although the effects of HMGS on downstream isoprenoid metabolites have been extensively reported, not much is known on how it might affect non-isoprenoid metabolic pathways. Here, the mechanism of F-244-mediated inhibition of primary root growth in Arabidopsis and the relationship between HMGS and non-isoprenoid metabolic pathways were investigated by untargeted SWATH-MS quantitative proteomics, quantitative real-time PCR, and target metabolite analysis. Our results revealed that the inhibition of primary root growth caused by F-244 was a consequence of reduced stigmasterol, auxin, and cytokinin levels. Interestingly, proteomic analyses identified a relationship between HMGS and glucosinolate biosynthesis. Inhibition of HMGS activated glucosinolate biosynthesis, resulting from the induction of glucosinolate biosynthesis-related genes, suppression of sterol biosynthesis-related genes, and reduction in sterol levels. In contrast, HMGS overexpression inhibited glucosinolate biosynthesis, due to down-regulation of glucosinolate biosynthesis-related genes, up-regulation of sterol biosynthesis-related genes, and increase in sterol content. Thus, HMGS might represent a target for the manipulation of glucosinolate biosynthesis, given the regulatory relationship between HMGS in the MVA pathway and glucosinolate biosynthesis.
机译：3-羟基-3-甲基戊芳基 - COA合酶（HMGS）催化甲羟戊酯（MVA）途径的第二步。据报道，HMGS抑制剂（F-244）延迟了小麦，烟草和芸苔juncea的生长，但该机制仍然未知。尽管HMGS对下游异戊二烯代谢物的影响已被广泛报道，但对于如何影响非异戊二烯代谢途径而言，并不多。这里，通过针对未明确的SWATH-MS定量蛋白质组学，定量实时PCR和靶代谢分析研究了F-244介导的拟拟拟拟拟拟拟拟拟拟拟拟征原生殖的机制和HMG和非异戊二烯代谢途径的关系。我们的研究结果表明，抑制由F-244引起的原发性根生长是降低脊柱甾醇，蟾蜍素和细胞素水平的结果。有趣的是，蛋白质组学分析确定了HMG和葡萄糖苷生物合成之间的关系。抑制HMGS活性葡糖苷生物合成，由胰酸葡萄糖酸酯生物合成相关基因的诱导，抑制甾醇生物合成相关基因以及甾醇水平的降低。相反，HMGS过表达抑制胰岛生物合成，由于葡萄糖苷生物合成相关基因的下调，甾醇生物合成相关基因的上调，并增加甾醇含量。因此，鉴于MVA途径和葡萄糖苷生物合成的HMG之间的调节关系，HMGS可能代表葡糖苷类生物合成的靶标。

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