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SLIM1 转录因子在拟南芥缺硫过程中影响糖信号转导。

The SLIM1 transcription factor affects sugar signaling during sulfur deficiency in Arabidopsis.

机构信息

Laboratory of Plant Protein Homeostasis, Institute of Biochemistry and Biophysics Polish Academy of Sciences, Warsaw, Poland.

Max Planck Institute of Molecular Plant Physiology, Am Mühlenberg 1, 14476, Potsdam-Golm, Germany.

出版信息

J Exp Bot. 2022 Dec 8;73(22):7362-7379. doi: 10.1093/jxb/erac371.

DOI:10.1093/jxb/erac371
PMID:36099003
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9730805/
Abstract

The homeostasis of major macronutrient metabolism needs to be tightly regulated, especially when the availability of one or more nutrients fluctuates in the environment. Both sulfur metabolism and glucose signaling are important processes throughout plant growth and development, as well as during stress responses. Still, very little is known about how these processes affect each other, although they are positively connected. Here, we showed in Arabidopsis that the crucial transcription factor of sulfur metabolism, SLIM1, is involved in glucose signaling during shortage of sulfur. The germination rate of the slim1_KO mutant was severely affected by high glucose and osmotic stress. The expression of SLIM1-dependent genes in sulfur deficiency appeared to be additionally induced by a high concentration of either mannitol or glucose, but also by sucrose, which is not only the source of glucose but another signaling molecule. Additionally, SLIM1 affects PAP1 expression during sulfur deficiency by directly binding to its promoter. The lack of PAP1 induction in such conditions leads to much lower anthocyanin production. Taken together, our results indicate that SLIM1 is involved in the glucose response by modulating sulfur metabolism and directly controlling PAP1 expression in Arabidopsis during sulfur deficiency stress.

摘要

主要宏量营养素代谢的动态平衡需要严格调控,尤其是当环境中一种或多种营养物质的供应发生波动时。硫代谢和葡萄糖信号转导都是植物生长发育以及应对胁迫反应过程中的重要过程。尽管它们之间存在正相关,但人们对这些过程如何相互影响知之甚少。在这里,我们在拟南芥中表明,硫代谢的关键转录因子 SLIM1 参与了硫饥饿时的葡萄糖信号转导。slim1_KO 突变体的萌发率受到高葡萄糖和渗透胁迫的严重影响。在缺硫条件下,依赖 SLIM1 的基因的表达似乎也被甘露醇或葡萄糖的高浓度额外诱导,但也被蔗糖诱导,蔗糖不仅是葡萄糖的来源,也是另一种信号分子。此外,SLIM1 通过直接结合其启动子来影响 PAP1 在缺硫条件下的表达。在这种情况下,PAP1 诱导的缺失会导致类黄酮的产生明显减少。总之,我们的结果表明,SLIM1 通过调节硫代谢参与葡萄糖反应,并在拟南芥缺硫胁迫期间直接控制 PAP1 的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/b54c51236534/erac371f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/b2732c212067/erac371f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/21e73f615318/erac371f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/12f1dd06bd94/erac371f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/0d17e9a2aac3/erac371f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/28787968a0c3/erac371f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/9b8e95735192/erac371f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/b54c51236534/erac371f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/b2732c212067/erac371f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/21e73f615318/erac371f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/12f1dd06bd94/erac371f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/0d17e9a2aac3/erac371f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/28787968a0c3/erac371f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/9b8e95735192/erac371f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e372/9730805/b54c51236534/erac371f0007.jpg

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