COP1 integrates light signals to ROP2 for cell cycle activation
COP1 integrates light signals to ROP2 for cell cycle activation
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DOI：
10.1080/15592324.2017.1363946
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发表时间：
2017-01-01
影响因子：
2.9
通讯作者：
Xiong, Yan
中科院分区：
文献类型：
--
作者：
Cai, Wenguo;Li, Xiaojuan;Xiong, Yan
植物茎尖细胞分裂受外界环境信号的精细调控，使植物能够适应不断变化的环境。我们最近已经表明，光直接信号和碳水化合物（糖）能量信号都是必不可少的细胞分裂在茎尖的激活。光被转化为生长素信号以激活小GT3 2（ROP 2）。随后，激活的ROP 2直接与雷帕霉素靶蛋白激酶（TOR）相互作用，这是细胞分裂的关键调节因子，以促进其激酶活性。然而，没有糖的存在，光和生长素都不能单独激活TOR激酶。在本附录中，我们发现组成型光形态发生1（COP 1）作为ROP 2的上游因子。COP 1以生长素依赖的方式调节ROP 2和TOR活性。cop 1 -6突变体在黑暗条件下真叶的发育受到生长素生物合成抑制剂yucasin和TOR化学抑制剂torin 2的影响。总之，我们的研究结果表明，COP 1调节生长素-ROP 2-TOR信号响应光。
The exquisite regulation of cell division at the shoot apex according to the external environmental cues enables plants to adapt the ever-changing environment. We have recently shown that light direct signaling and carbohydrate (sugar) energy signaling are both essential for the activation of cell division at the shoot apex. Light is converted to auxin signal to activate small GTPase 2 (ROP2). Subsequently, the activated ROP2 directly interacts with Target of Rapamycin (TOR) protein kinase, a pivotal regulator of cell division, to promote its kinase activity. However, neither light nor auxin alone can activate TOR kinase without the presence of sugar. In this addendum, we showed that Constitutive Photomorphogenesis 1 (COP1) acts as an upstream factor of ROP2. COP1 regulates ROP2 and TOR activity in an auxin dependent manner. The development of true leaves in the cop1-6 mutant under darkness is compromised by auxin biosynthesis inhibitor yucasin and TOR chemical inhibitor torin2. Together, our results suggested that COP1 regulates auxin-ROP2-TOR signaling in response to light.