The Arabidopsis RING-type E3 Ligase TEAR1 Controls Leaf Development by Targeting the TIE1 Transcriptional Repressor for Degradation.
The Arabidopsis RING-type E3 Ligase TEAR1 Controls Leaf Development by Targeting the TIE1 Transcriptional Repressor for Degradation.
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拟南芥 RING 型 E3 连接酶 TEAR1 通过靶向 TIE1 转录阻遏蛋白降解来控制叶片发育。
DOI：
10.1105/tpc.16.00771
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发表时间：
2017
期刊：
影响因子：
11.6
通讯作者：
Qin Genji
中科院分区：
文献类型：
--
作者：
Zhang Jinzhe;Wei Baoye;Yuan Rongrong;Wang Jianhui;Ding Mingxin;Chen Zhuoyao;Yu Hao;Qin Genji
叶片大小和形状的发育可塑性对叶片功能和植物存活具有重要意义。然而，植物响应环境条件形成不同叶子的机制还没有很好的理解。在这里，我们确定了TIE 1相关环型E3连接酶1（TEAR 1），并发现它通过促进含TCP相互作用基序蛋白1（TIE 1）的降解来调节叶发育，TIE 1是肉桂（CIN）样TEOSINTE BRANCHED 1/CYCLOIDEA/PCF（TCP）转录因子的重要阻遏物，而这些转录因子是叶发育的关键。TEAR 1含有典型的C3 H2 C3型RING结构域，具有E3连接酶活性。我们发现TEAR 1与TCP阻遏物TIE 1相互作用，TIE 1在体内被泛素化并被26 S蛋白酶体系统降解。我们证明TEAR 1与TIE 1共定位于细胞核中，并负调控TIE 1蛋白水平。TEAR 1的过表达挽救了由TIE 1过表达引起的叶片缺陷，而TEAR 1的破坏导致了类似于由TIE 1过表达或TCP功能障碍引起的叶片表型。TEAR的缺失部分挽救了TCP 4过表达系的叶片缺陷，并增强了jaw-5D的波浪叶表型。我们认为TEAR 1通过介导TCP阻遏物TIE 1的降解来积极调节类CIN TCP活性以促进叶片发育。
The developmental plasticity of leaf size and shape is important for leaf function and plant survival. However, the mechanisms by which plants form diverse leaves in response to environmental conditions are not well understood. Here, we identified TIE1-ASSOCIATED RING-TYPE E3 LIGASE1 (TEAR1) and found that it regulates leaf development by promoting the degradation of TCP INTERACTOR-CONTAINING EAR MOTIF PROTEIN1 (TIE1), an important repressor of CINCINNATA (CIN)-like TEOSINTE BRANCHED1/CYCLOIDEA/PCF (TCP) transcription factors, which are key for leaf development. TEAR1 contains a typical C3H2C3-type RING domain and has E3 ligase activity. We show that TEAR1 interacts with the TCP repressor TIE1, which is ubiquitinated in vivo and degraded by the 26S proteasome system. We demonstrate that TEAR1 is colocalized with TIE1 in nuclei and negatively regulates TIE1 protein levels. Overexpression ofTEAR1rescued leaf defects caused byTIE1overexpression, whereas disruption of TEAR1 resulted in leaf phenotypes resembling those caused byTIE1overexpression or TCP dysfunction. Deficiency inTEARpartially rescued the leaf defects ofTCP4overexpression line and enhanced the wavy leaf phenotypes ofjaw-5D. We propose that TEAR1 positively regulates CIN-like TCP activity to promote leaf development by mediating the degradation of the TCP repressor TIE1.