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数学建模揭示,蔗糖通过动态糖信号通路调控叶片衰老。

Mathematical Modeling Reveals That Sucrose Regulates Leaf Senescence via Dynamic Sugar Signaling Pathways.

机构信息

Key Laboratory of Tobacco Biology and Processing, Ministry of Agriculture and Rural Affairs, Tobacco Research Institute, Chinese Academy of Agricultural Sciences, Qingdao 266101, China.

State Key Laboratory of Subtropical Silviculture, Zhejiang A&F University, 666 Wusu Street, Hangzhou 311300, China.

出版信息

Int J Mol Sci. 2022 Jun 10;23(12):6498. doi: 10.3390/ijms23126498.

Abstract

Sucrose (Suc) accumulation is one of the key indicators of leaf senescence onset, but little is known about its regulatory role. Here, we found that application of high (120-150 mM) and low levels (60 mM) of Suc to young leaf (YL) and fully expanded leaf (FEL) discs, respectively, decreased chlorophyll content and maximum photosynthetic efficiency. Electrolyte leakage and malondialdehyde levels increased at high Suc concentrations (90-120 mM in YL and 60 and 150 mM in FEL discs). In FEL discs, the senescence-associated gene showed a gradual increase in expression with increased Suc application; in contrast, in YL discs, was upregulated with low Suc treatment (60 mM) but downregulated at higher levels of Suc. In YL discs, trehalose-6-phosphate (T6P) accumulated at a low half-maximal effective concentration (EC50) of Suc (1.765 mM). However, T6P levels declined as trehalose 6 phosphate synthase (TPS) content decreased, resulting in the maximum velocity of sucrose non-fermenting-1-related protein kinase (SnRK) and hexokinase (HXK) occurring at higher level of Suc. We therefore speculated that senescence was induced by hexose accumulation. In FEL discs, the EC50 of T6P occurred at a low concentration of Suc (0.9488 mM); T6P levels progressively increased with higher TPS content, which inhibited SnRK activity with a dissociation constant () of 0.001475 U/g. This confirmed that the T6P-SnRK complex induced senescence in detached FEL discs.

摘要

蔗糖(Suc)积累是叶片衰老开始的关键指标之一,但对其调控作用知之甚少。在这里,我们发现分别将高浓度(120-150mM)和低浓度(60mM)的蔗糖应用于幼叶(YL)和完全展开的叶片(FEL)圆盘,会降低叶绿素含量和最大光合作用效率。在高蔗糖浓度(YL 中的 90-120mM 和 FEL 中的 60 和 150mM)下,电解质渗漏和丙二醛水平增加。在 FEL 圆盘,衰老相关基因随着蔗糖应用的增加逐渐表达增加;相反,在 YL 圆盘,低浓度蔗糖处理(60mM)上调,但在较高水平的蔗糖下调。在 YL 圆盘,海藻糖-6-磷酸(T6P)在蔗糖的低半最大有效浓度(EC50)(1.765mM)下积累。然而,随着海藻糖 6 磷酸合酶(TPS)含量的降低,T6P 水平下降,导致蔗糖非发酵-1 相关蛋白激酶(SnRK)和己糖激酶(HXK)的最大速度在更高水平的蔗糖下发生。因此,我们推测衰老是由己糖积累引起的。在 FEL 圆盘,T6P 的 EC50 出现在蔗糖的低浓度(0.9488mM);T6P 水平随着 TPS 含量的增加而逐渐增加,这抑制了 SnRK 活性,解离常数()为 0.001475U/g。这证实了 T6P-SnRK 复合物诱导了离体 FEL 圆盘的衰老。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9506/9223756/672a63d00e12/ijms-23-06498-g001.jpg

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