Zhang Jinzhe, Wei Baoye, Yuan Rongrong, Wang Jianhui, Ding Mingxin, Chen Zhuoyao, Yu Hao, Qin Genji
State Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing 100871, People's Republic of China.
State Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing 100871, People's Republic of China
Plant Cell. 2017 Feb;29(2):243-259. doi: 10.1105/tpc.16.00771. Epub 2017 Jan 18.
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 of rescued leaf defects caused by overexpression, whereas disruption of TEAR1 resulted in leaf phenotypes resembling those caused by overexpression or TCP dysfunction. Deficiency in partially rescued the leaf defects of overexpression line and enhanced the wavy leaf phenotypes of We propose that TEAR1 positively regulates CIN-like TCP activity to promote leaf development by mediating the degradation of the TCP repressor TIE1.
叶片大小和形状的发育可塑性对于叶片功能和植物存活至关重要。然而，植物如何响应环境条件形成多样叶片的机制尚不清楚。在这里，我们鉴定了与TIE1相关的环型E3连接酶1（TEAR1），并发现它通过促进含TCP相互作用基序的EAR基序蛋白1（TIE1）的降解来调节叶片发育，TIE1是CINCINNATA（CIN）样TEOSINTE BRANCHED1/CYCLOIDEA/PCF（TCP）转录因子的重要抑制因子，而这些转录因子对叶片发育至关重要。TEAR1含有典型的C3H2C3型环结构域并具有E3连接酶活性。我们表明TEAR1与TCP抑制因子TIE1相互作用，TIE1在体内被泛素化并被26S蛋白酶体系统降解。我们证明TEAR1与TIE1在细胞核中共定位并负向调节TIE1蛋白水平。TEAR1的过表达挽救了由TIE1过表达引起的叶片缺陷，而TEAR1的破坏导致叶片表型类似于由TIE1过表达或TCP功能障碍引起的表型。TIE1的缺失部分挽救了TIE1过表达系的叶片缺陷并增强了TIE1的波浪叶表型。我们提出TEAR1通过介导TCP抑制因子TIE1的降解来正向调节CIN样TCP活性以促进叶片发育。
