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在拟南芥中,AtMYBS1 通过直接抑制 MAX1 的表达来负调控热胁迫耐性,而 MAX1 是合成独脚金内酯所必需的。

AtMYBS1 negatively regulates heat tolerance by directly repressing the expression of MAX1 required for strigolactone biosynthesis in Arabidopsis.

机构信息

Collaborative Innovation Center of Henan Grain Crops, College of Agronomy, Henan Agricultural University, Zhengzhou 450002, China; Key Laboratory of Biology and Genetic Improvement of Oil Crops, the Ministry of Agriculture and Rural Affairs, Oil Crops Research Institute of Chinese Academy of Agricultural Sciences, Wuhan 430062, China; Xinxiang Academy of Agricultural Sciences, Xinxiang 453000, China.

Key Laboratory of Biology and Genetic Improvement of Oil Crops, the Ministry of Agriculture and Rural Affairs, Oil Crops Research Institute of Chinese Academy of Agricultural Sciences, Wuhan 430062, China.

出版信息

Plant Commun. 2023 Nov 13;4(6):100675. doi: 10.1016/j.xplc.2023.100675. Epub 2023 Aug 22.

DOI:10.1016/j.xplc.2023.100675
PMID:37608548
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10721535/
Abstract

Heat stress caused by global warming requires the development of thermotolerant crops to sustain yield. It is necessary to understand the molecular mechanisms that underlie heat tolerance in plants. Strigolactones (SLs) are a class of carotenoid-derived phytohormones that regulate plant development and responses to abiotic or biotic stresses. Although SL biosynthesis and signaling processes are well established, genes that directly regulate SL biosynthesis have rarely been reported. Here, we report that the MYB-like transcription factor AtMYBS1/AtMYBL, whose gene expression is repressed by heat stress, functions as a negative regulator of heat tolerance by directly inhibiting SL biosynthesis in Arabidopsis. Overexpression of AtMYBS1 led to heat hypersensitivity, whereas atmybs1 mutants displayed increased heat tolerance. Expression of MAX1, a critical enzyme in SL biosynthesis, was induced by heat stress and downregulated in AtMYBS1-overexpression (OE) plants but upregulated in atmybs1 mutants. Overexpression of MAX1 in the AtMYBS1-OE background reversed the heat hypersensitivity of AtMYBS1-OE plants. Loss of MAX1 function in the atmyb1 background reversed the heat-tolerant phenotypes of atmyb1 mutants. Yeast one-hybrid assays, chromatin immunoprecipitation‒qPCR, and transgenic analyses demonstrated that AtMYBS1 directly represses MAX1 expression through the MYB binding site in the MAX1 promoter in vivo. The atmybs1d14 double mutant, like d14 mutants, exhibited hypersensitivity to heat stress, indicating the necessary role of SL signaling in AtMYBS1-regulated heat tolerance. Our findings provide new insights into the regulatory network of SL biosynthesis, facilitating the breeding of heat-tolerant crops to improve crop production in a warming world.

摘要

全球变暖导致的热应激要求开发耐热作物以维持产量。有必要了解植物耐热性的分子机制。独脚金内酯(SLs)是一类由类胡萝卜素衍生的植物激素,调节植物发育和对非生物或生物胁迫的反应。尽管 SL 的生物合成和信号转导过程已经得到很好的阐明,但直接调节 SL 生物合成的基因很少被报道。在这里,我们报告 MYB 样转录因子 AtMYBS1/AtMYBL,其基因表达受热应激抑制,通过直接抑制拟南芥 SL 生物合成,作为耐热性的负调控因子发挥作用。AtMYBS1 的过表达导致热敏感,而 atmybs1 突变体表现出增强的耐热性。SL 生物合成的关键酶 MAX1 的表达受热应激诱导,并在 AtMYBS1 过表达(OE)植物中下调,但在 atmybs1 突变体中上调。在 AtMYBS1-OE 背景下过表达 MAX1 逆转了 AtMYBS1-OE 植物的热敏感表型。在 atmyb1 背景下缺失 MAX1 功能逆转了 atmyb1 突变体的耐热表型。酵母单杂交试验、染色质免疫沉淀-qPCR 和转基因分析表明,AtMYBS1 通过 MAX1 启动子中的 MYB 结合位点在体内直接抑制 MAX1 的表达。与 d14 突变体一样,atmybs1d14 双突变体对热应激表现出敏感性,表明 SL 信号在 AtMYBS1 调节的耐热性中具有必要的作用。我们的发现为 SL 生物合成的调控网络提供了新的见解,有助于培育耐热作物,以提高变暖世界中的作物产量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/2ffdfdda61f8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/ad110d1feefc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/bde009269e7d/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/88e0f5a9c343/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/028f72600c77/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/2ffdfdda61f8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/ad110d1feefc/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/bde009269e7d/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/88e0f5a9c343/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/028f72600c77/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c6f/10721535/2ffdfdda61f8/gr5.jpg

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