Short-term inhibition of glutamine synthetase leads to reprogramming of amino acid and lipid metabolism in roots and leaves of tea plant (Camellia sinensis L.)

文献类型： 外文期刊

第一作者： Liu, Mei-Ya

作者： Liu, Mei-Ya;Tang, Dandan;Shi, Yuanzhi;Ma, Lifeng;Zhang, Qunfeng;Ruan, Jianyun;Li, Yan

作者机构：

关键词： Glutamine synthetase; Methionine sulfoximine; Quality-related compounds; Amino acids; Lipids; Tea plant

期刊名称：BMC PLANT BIOLOGY （ 影响因子：4.215； 五年影响因子：4.96 ）

ISSN： 1471-2229

年卷期： 2019 年 19 卷 1 期

页码：

收录情况： SCI

摘要： Background Nitrogen (N) nutrition significantly affected metabolism and accumulation of quality-related compounds in tea plant (Camellia sinensis L.). Little is known about the physiological and molecular mechanisms underlying the effects of short-term repression of N metabolism on tea roots and leaves for a short time. Results In this study, we subjected tea plants to a specific inhibitor of glutamine synthetase (GS), methionine sulfoximine (MSX), for a short time (30 min) and investigated the effect of the inhibition of N metabolism on the transcriptome and metabolome of quality-related compounds. Our results showed that GS activities in tea roots and leaves were significantly inhibited upon MSX treatment, and both tissue types showed a sensitive metabolic response to GS inhibition. In tea leaves, the hydrolysis of theanine decreased with the increase in theanine and free ammonium content. The biosynthesis of all other amino acids was repressed, and the content of N-containing lipids declined, suggesting that short-term inhibition of GS reduces the level of N reutilization in tea leaves. Metabolites related to glycolysis and the tricarboxylic acid (TCA) cycle accumulated after GS repression, whereas the content of amino acids such as glycine, serine, isoleucine, threonine, leucine, and valine declined in the MXS treated group. We speculate that the biosynthesis of amino acids is affected by glycolysis and the TCA cycle in a feedback loop. Conclusions Overall, our data suggest that GS repression in tea plant leads to the reprogramming of amino acid and lipid metabolic pathways.

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