Zhang Zhenzhen, Zhu Jia-Ying, Roh Jeehee, Marchive Chloé, Kim Seong-Ki, Meyer Christian, Sun Yu, Wang Wenfei, Wang Zhi-Yong
Hebei Key Laboratory of Molecular and Cellular Biology, Key Laboratory of Molecular and Cellular Biology of Ministry of Education, College of Life Science, Hebei Normal University, Hebei Collaboration Innovation Center for Cell Signaling, Shijiazhuang, Hebei 050024, China; Center of Basic Forestry and Proteomics, Haixia Institute of Science and Technology (HIST), Fujian Agriculture and Forestry University (FAFU), Fuzhou 350002, China.
Department of Plant Biology, Carnegie Institution for Science, Stanford, CA 94305, USA.
Curr Biol. 2016 Jul 25;26(14):1854-60. doi: 10.1016/j.cub.2016.05.005. Epub 2016 Jun 23.
For maintenance of cellular homeostasis, the actions of growth-promoting hormones must be attenuated when nutrient and energy become limiting. The molecular mechanisms that coordinate hormone-dependent growth responses with nutrient availability remain poorly understood in plants [1, 2]. The target of rapamycin (TOR) kinase is an evolutionarily conserved master regulator that integrates nutrient and energy signaling to regulate growth and homeostasis in both animals and plants [3-7]. Here, we show that sugar signaling through TOR controls the accumulation of the brassinosteroid (BR)-signaling transcription factor BZR1, which is essential for growth promotion by multiple hormonal and environmental signals [8-11]. Starvation, caused by shifting of light-grown Arabidopsis seedlings into darkness, as well as inhibition of TOR by inducible RNAi, led to plant growth arrest and reduced expression of BR-responsive genes. The growth arrest caused by TOR inactivation was partially recovered by BR treatment and the gain-of-function mutation bzr1-1D, which causes accumulation of active forms of BZR1 [12]. Exogenous sugar promoted BZR1 accumulation and seedling growth, but such sugar effects were largely abolished by inactivation of TOR, whereas the effect of TOR inactivation on BZR1 degradation is abolished by inhibition of autophagy and by the bzr1-1D mutation. These results indicate that cellular starvation leads sequentially to TOR inactivation, autophagy, and BZR1 degradation. Such regulation of BZR1 accumulation by glucose-TOR signaling allows carbon availability to control the growth promotion hormonal programs, ensuring supply-demand balance in plant growth.
为维持细胞内稳态，当营养物质和能量供应受限的时候，促生长激素的作用必须被减弱。在植物中，协调激素依赖型生长反应与营养物质可利用性之间关系的分子机制仍知之甚少[1,2]。雷帕霉素靶蛋白（TOR）激酶是一种在进化上保守的主要调节因子，它整合营养和能量信号，以调节动物和植物的生长及内稳态[3-7]。在这里，我们表明通过TOR的糖信号传导控制油菜素内酯（BR）信号转录因子BZR1的积累，BZR1对于多种激素和环境信号促进生长至关重要[8-11]。将光照培养的拟南芥幼苗转移到黑暗中导致的饥饿，以及通过诱导RNA干扰抑制TOR，都会导致植物生长停滞，并降低BR响应基因的表达。BR处理和功能获得性突变bzr1-1D（该突变导致BZR1活性形式的积累[12]）部分恢复了由TOR失活引起的生长停滞。外源糖促进了BZR1的积累和幼苗生长，但这种糖效应在很大程度上被TOR失活所消除，而自噬抑制和bzr1-1D突变消除了TOR失活对BZR1降解的影响。这些结果表明，细胞饥饿会依次导致TOR失活、自噬和BZR1降解。葡萄糖-TOR信号传导对BZR1积累的这种调节使碳的可利用性能够控制促进生长的激素程序，确保植物生长中的供需平衡。
