TOR Signaling Promotes Accumulation of BZR1 to Balance Growth with Carbon Availability in Arabidopsis.

TOR Signaling Promotes Accumulation of BZR1 to Balance Growth with Carbon Availability in Arabidopsis.
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DOI:
10.1016/j.cub.2016.05.005
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发表时间:
2016-07-25
期刊:
影响因子:
9.2
通讯作者:
Wang, Zhi-Yong
Wang, Zhi-Yong
中科院分区:
生物学1区
文献类型:
--
作者:
Zhang, Zhenzhen;Zhu, Jia-Ying;Roh, Jeehee;Marchive, Chloe;Kim, Seong-Ki;Meyer, Christian;Sun, Yu;Wang, Wenfei;Wang, Zhi-Yong

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为了维持细胞稳态,当营养和能量受到限制时,促生长激素的作用必须减弱。在植物中,协调激素依赖性生长反应与养分可用性的分子机制仍然知之甚少。雷帕霉素靶标 (TOR) 激酶是一种进化上保守的主调节因子,它整合营养和能量信号来调节动物和植物的生长和体内平衡。在这里,我们发现通过 TOR 的糖信号传导控制油菜素类固醇 (BR) 信号转录因子 BZR1 的积累,这对于多种激素和环境信号促进生长至关重要。将光照生长的拟南芥幼苗转移到黑暗中引起的饥饿,以及诱导性 RNAi 对 TOR 的抑制,导致植物生长停滞并减少 BR 响应基因的表达。 TOR 失活引起的生长停滞可通过 BR 处理和功能获得突变 bzr1-1D 部分恢复,这会导致 BZR1 活性形式的积累。外源糖促进了 BZR1 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 TOR 失活对 BZR1 降解的影响则被自噬抑制和 bzr1-1D 突变所消除。这些结果表明细胞饥饿会依次导致 TOR 失活、自噬和 BZR1 降解。这种通过葡萄糖-TOR信号传导对BZR1积累的调节允许碳的可用性来控制生长促进激素程序,确保植物生长的供需平衡。
To maintain 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. 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. 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. Starvation, caused by shifting 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. 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.
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