The Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao 266237, China.
Shandong Provincial Key Laboratory of Plant Stress, College of Life Sciences, Shandong Normal University, Jinan 250014, China.
Plant Cell. 2022 Mar 4;34(3):1038-1053. doi: 10.1093/plcell/koab307.
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 β-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.
淀粉是植物中主要的储能碳水化合物，是植物代谢和在不断变化的环境条件下生长的重要碳储存分子。雷帕霉素靶蛋白（TOR）激酶是一种进化上保守的主要调节剂，它整合能量、营养、激素和应激信号，以调节所有真核生物的生长。在这里，我们证明 TOR 促进保卫细胞淀粉降解并诱导拟南芥气孔开放。在短光照或低光照光子辐照下生长的植物以及 TOR 失活引起的饥饿会损害保卫细胞淀粉降解和气孔开放。糖和 TOR 诱导β-淀粉酶 1（BAM1）的积累，BAM1 负责保卫细胞中的淀粉降解。植物甾体激素油菜素内酯和转录因子 BRASSINAZOLE-RESISTANT1 在糖促进 BAM1 表达中起关键作用。此外，糖供应诱导 BAM1 积累，但 TOR 失活导致 BAM1 降解，并且通过抑制自噬和蛋白酶体途径或通过 BAM1 丝氨酸-31 的磷酸模拟突变，TOR 失活对 BAM1 降解的影响被消除。这种由糖-TOR 信号调节的 BAM1 活性允许碳可用性来调节保卫细胞淀粉代谢和气孔运动，从而确保植物的最佳光合作用效率。
