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

作　　者：Xiang Li Jianhua Lu Xuling Zhu Yanqi Dong Yanli Liu Shanshan Chu Erhui Xiong Xu Zheng Yongqing Jiao 

机构地区：[1]Collaborative Innovation Center of Henan Grain Crops,College of Agronomy,Henan Agricultural University,Zhengzhou 450002,China [2]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 [3]Xinxiang Academy of Agricultural Sciences,Xinxiang 453000,China

出　　处：《Plant Communications》2023年第6期134-147,共14页植物通讯（英文）

基　　金：supported by Henan Agricultural University(30500689).

摘　　要：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.

关 键 词：atmybs1 MAX1 STRIGOLACTONE heat MYB D14 

分 类 号：Q94[生物学—植物学]