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TOR promotes guard cell starch degradation by regulating the activity of β-AMYLASE1 in Arabidopsis

文献类型：期刊论文

作者Han, Chao; Hua, Wenbo; Li, Jinge1; Qiao, Yan; Yao, Lianmei; Hao, Wei; Li, Ruizi5; Fan, Min; De Jaeger, Geert3,4; Yang, Wenqiang5
刊名PLANT CELL
出版日期2022
卷号34期号:3页码:1038-1053
ISSN号1040-4651
DOI10.1093/plcell/koab307
文献子类Article
英文摘要TOR promotes BAM1 expression through BZR1, and induces BAM1 accumulation by inhibiting the autophagy and proteasome pathways, thereby promoting guard cell starch degradation and stomatal opening. Starch is the main energy storage carbohydrate in plants and serves as an essential carbon storage molecule for plant metabolism and growth under changing environmental conditions. The TARGET of RAPAMYCIN (TOR) kinase is an evolutionarily conserved master regulator that integrates energy, nutrient, hormone, and stress signaling to regulate growth in all eukaryotes. Here, we demonstrate that TOR promotes guard cell starch degradation and induces stomatal opening in Arabidopsis thaliana. Starvation caused by plants growing under short photoperiod or low light photon irradiance, as well as inactivation of TOR, impaired guard cell starch degradation and stomatal opening. Sugar and TOR induce the accumulation of beta-AMYLASE1 (BAM1), which is responsible for starch degradation in guard cells. The plant steroid hormone brassinosteroid and transcription factor BRASSINAZOLE-RESISTANT1 play crucial roles in sugar-promoted expression of BAM1. Furthermore, sugar supply induced BAM1 accumulation, but TOR inactivation led to BAM1 degradation, and the effects of TOR inactivation on BAM1 degradation were abolished by the inhibition of autophagy and proteasome pathways or by phospho-mimicking mutation of BAM1 at serine-31. Such regulation of BAM1 activity by sugar-TOR signaling allows carbon availability to regulate guard cell starch metabolism and stomatal movement, ensuring optimal photosynthesis efficiency of plants.
学科主题Biochemistry & Molecular Biology ; Plant Sciences ; Cell Biology
电子版国际标准刊号1532-298X
出版地CARY
WOS关键词STOMATAL CLOSURE ; GROWTH ; METABOLISM ; GLUCOSE ; TARGET ; LIGHT ; NUTRIENT ; HXK1 ; BZR1
WOS研究方向Science Citation Index Expanded (SCI-EXPANDED)
语种英语
出版者OXFORD UNIV PRESS INC
WOS记录号WOS:000764265700011
资助机构National Natural Science Foundation of China [31600199, 31670284, 31970306, 31870262] ; Science and Technology Department of Shandong Province [2019LZGC015, ZR2019ZD16]
源URL[http://ir.ibcas.ac.cn/handle/2S10CLM1/28469]  
专题中科院光生物学重点实验室
作者单位1.Shandong Univ, Sch Life Sci, Minist Educ, Key Lab Plant Dev & Environm Adaptat Biol, Qingdao 266237, Peoples R China
2.VIB Ctr Plant Syst Biol, Ghent, Belgium
3.Univ Ghent, Dept Plant Biotechnol & Bioinformat, Ghent, Belgium
4.Chinese Acad Sci, Inst Bot, Key Lab Photobiol, Beijing, Peoples R China
5.Shandong Normal Univ, Coll Life Sci, Shandong Prov Key Lab Plant Stress, Jinan 250014, Peoples R China
推荐引用方式
GB/T 7714		 Han, Chao,Hua, Wenbo,Li, Jinge,et al. TOR promotes guard cell starch degradation by regulating the activity of β-AMYLASE1 in Arabidopsis[J]. PLANT CELL,2022,34(3):1038-1053.
APA Han, Chao.,Hua, Wenbo.,Li, Jinge.,Qiao, Yan.,Yao, Lianmei.,...&Bai, Ming-Yi.(2022).TOR promotes guard cell starch degradation by regulating the activity of β-AMYLASE1 in Arabidopsis.PLANT CELL,34(3),1038-1053.
MLA Han, Chao,et al."TOR promotes guard cell starch degradation by regulating the activity of β-AMYLASE1 in Arabidopsis".PLANT CELL 34.3(2022):1038-1053.

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来源：植物研究所

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