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TOR–EIN2信号轴介导核信号来调节植物生长
2021-03-07 21:43

福建农林大学熊延团队发现,TOR–EIN2信号轴介导核信号来调节植物生长。这一研究成果于2021年3月3日在线发表在国际学术期刊《自然》上。

研究人员发现,乙烯不敏感蛋白2(EIN2),一个在细胞质和细胞核之间穿梭的核心整合因子,是拟南芥中雷帕霉素靶标(TOR)的直接底物。葡萄糖激活的TOR激酶直接磷酸化EIN2,以防止其核定位。值得注意的是,在Ein2-5突变体中,由葡萄糖-TOR信号引导的快速全局转录重编程受到很大影响,而EIN2负调控与DNA复制有关的各种葡萄糖激活TOR靶基因的表达、细胞壁和脂质合成以及各种次级代谢途径。

化学、细胞和遗传分析表明,受葡萄糖–TOR–EIN2信号轴控制的细胞伸长和增殖过程与典型的乙烯–CTR1–EIN2信号解耦,并由不同的磷酸化位点介导。这些发现揭示了一种新的分子机制,通过该机制可以共享一个中央信号传导枢纽,但可以使用上游蛋白激酶介导的不同磷酸化编码,从而通过多种信号传导途径来实现差异性调节。 

据悉,进化保守的TOR激酶通过整合所有真核生物中的营养、能量、激素和应激信号,来充当协调细胞增殖和生长的主要调节因子。研究主要集中在TOR调控的翻译上,但是TOR如何协调全局转录网络仍不清楚。

附:英文原文

Title: The TOR–EIN2 axis mediates nuclear signalling to modulate plant growth

Author: Liwen Fu, Yanlin Liu, Guochen Qin, Ping Wu, Hailing Zi, Zhongtian Xu, Xiaodi Zhao, Yue Wang, Yaxing Li, Shuhui Yang, Chao Peng, Catherine C. L. Wong, Sang-Dong Yoo, Zecheng Zuo, Renyi Liu, Young-Hee Cho, Yan Xiong

Issue&Volume: 2021-03-03

Abstract: 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 eukaryotes1,2. 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 integrator3,4,5 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.

DOI: 10.1038/s41586-021-03310-y

Source: https://www.nature.com/articles/s41586-021-03310-y

Nature:《自然》,创刊于1869年。隶属于施普林格·自然出版集团,最新IF:69.504
官方网址:http://www.nature.com/
投稿链接:http://www.nature.com/authors/submit_manuscript.html


本期文章:《自然》:Online/在线发表

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