The TOR-EIN2 axis mediates nuclear signalling to modulate plant growth
The TOR-EIN2 axis mediates nuclear signalling to modulate plant growth
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TOR-EIN2 轴介导核信号传导以调节植物生长
DOI：
10.1038/s41586-021-03310-y
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发表时间：
2021-03-03
期刊：
影响因子：
64.8
通讯作者：
Xiong, Yan
中科院分区：
文献类型：
--
作者：
Fu, Liwen;Liu, Yanlin;Xiong, Yan
雷帕霉素(TOR)激酶是进化上保守的靶标，通过整合所有真核生物中的营养、能量、激素和应激信号来协调细胞的增殖和生长(1，2)。研究主要集中在TOR调控的翻译上，但TOR如何协调全球转录网络仍不清楚。在这里，我们确定乙烯不敏感蛋白2(EIN2)，一个穿梭于细胞质和细胞核之间的中央整合子(3-5)，是拟南芥TOR的直接底物。葡萄糖激活的TOR激酶直接磷酸化EIN2以阻止其核定位。值得注意的是，在ein2-5突变体中，由葡萄糖-TOR信号指导的快速全球转录重编程在很大程度上受到了损害，EIN2负面调节了葡萄糖激活的TOR的一系列靶基因的表达，这些基因参与了DNA复制、细胞壁和脂肪合成以及各种次生代谢途径。化学、细胞和遗传学分析表明，由葡萄糖-TOR-EIN2轴控制的细胞伸长和增殖过程与典型的乙烯-CTR1-EIN2信号解偶联，并由不同的磷酸化位点介导。我们的发现揭示了一种分子机制，通过这种机制，中央信号中心是共享的，但不同的信号通路使用不同的磷酸化代码进行差异调制，这些代码可以由上游蛋白激酶指定。
The evolutionarily conserved target of rapamycin (TOR) kinase acts as a master regulator that coordinates cell proliferation and growth by integrating nutrient, energy, hormone and stress signals in all eukaryotes(1,2). Research has focused mainly on TOR-regulated translation, but how TOR orchestrates the global transcriptional network remains unclear. Here we identify ethylene-insensitive protein 2 (EIN2), a central integrator(3-5) that shuttles between the cytoplasm and the nucleus, as a direct substrate of TOR in Arabidopsis thaliana. Glucose-activated TOR kinase directly phosphorylates EIN2 to prevent its nuclear localization. Notably, the rapid global transcriptional reprogramming that is directed by glucose-TOR signalling is largely compromised in the ein2-5 mutant, and EIN2 negatively regulates the expression of a wide range of target genes of glucose-activated TOR that are involved in DNA replication, cell wall and lipid synthesis and various secondary metabolic pathways. Chemical, cellular and genetic analyses reveal that cell elongation and proliferation processes that are controlled by the glucose-TOR-EIN2 axis are decoupled from canonical ethylene-CTR1-EIN2 signalling, and mediated by different phosphorylation sites. Our findings reveal a molecular mechanism by which a central signalling hub is shared but differentially modulated by diverse signalling pathways using distinct phosphorylation codes that can be specified by upstream protein kinases.