北京大学生命科学学院近日在国际知名学术期刊Plant Cell在线发表其最新研究成果。
郭红卫教授课题组研究了乙烯如何抑制了转录因子EIN3/EIL1蛋白降解。该实验室一直致力于乙烯信号转导的具体生化机理研究。早在2003年，郭红卫教授报道了植物激素乙烯能促进重要的转录因子EIN3的蛋白积累，而在没有乙烯的情况下，EIN3被两个F-Box EBF1/EBF2所降解（Guo and Ecker, Cell, 2003），但是乙烯是如何抑制EIN3蛋白降解的仍无明确答案。
本研究结果发现EIN3的同源基因EIL1也介导了乙烯反应，并也被BF1/EBF2所降解，EIN2和EBF1/EBF2位于EIN3/EIL1遗传学上游。进一步研究发现乙烯能诱导EBF1/EBF2蛋白降解，进而稳定了EIN3/EIL1，且该过程要求存在EIN2。这是植物激素调控F-Box蛋白降解作为关键信号机制的首次报道，将对其他F-Box在多个激素信号途径的调控机理提供重要借鉴意义。
生物谷推荐原文出处：
The Plant Cell doi：10.1105/tpc.110.076588
Ethylene-Induced Stabilization of ETHYLENE INSENSITIVE3 and EIN3-LIKE1 Is Mediated by Proteasomal Degradation of EIN3 Binding F-Box 1 and 2 That Requires EIN2 in Arabidopsis[C],[W]
Fengying Ana,1, Qiong Zhaoa,1, Yusi Jia, Wenyang Lia, Zhiqiang Jianga, Xiangchun Yua, Chen Zhanga, Ying Hana, Wenrong Hea, Yidong Liub, Shuqun Zhangb, Joseph R. Eckerc and Hongwei Guoa,2
a National Laboratory of Protein Engineering and Plant Genetic Engineering, College of Life Sciences, Peking University, Beijing 100871, China
b Division of Biochemistry and Bond Life Sciences Center, University of Missouri, Columbia, Missouri, 65211
c Plant Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037
Plant responses to ethylene are mediated by regulation of EBF1/2-dependent degradation of the ETHYLENE INSENSITIVE3 (EIN3) transcription factor. Here, we report that the level of EIL1 protein is upregulated by ethylene through an EBF1/2-dependent pathway. Genetic analysis revealed that EIL1 and EIN3 cooperatively but differentially regulate a wide array of ethylene responses, with EIL1 mainly inhibiting leaf expansion and stem elongation in adult plants and EIN3 largely regulating a multitude of ethylene responses in seedlings. When EBF1 and EBF2 are disrupted, EIL1 and EIN3 constitutively accumulate in the nucleus and remain unresponsive to exogenous ethylene application. Further study revealed that the levels of EBF1 and EBF2 proteins are downregulated by ethylene and upregulated by silver ion and MG132, suggesting that ethylene stabilizes EIN3/EIL1 by promoting EBF1 and EBF2 proteasomal degradation. Also, we found that EIN2 is indispensable for mediating ethylene-induced EIN3/EIL1 accumulation and EBF1/2 degradation, whereas MKK9 is not required for ethylene signal transduction, contrary to a previous report. Together, our studies demonstrate that ethylene similarly regulates EIN3 and EIL1, the two master transcription factors coordinating myriad ethylene responses, and clarify that EIN2 but not MKK9 is required for ethylene-induced EIN3/EIL1 stabilization. Our results also reveal that EBF1 and EBF2 act as essential ethylene signal transducers that by themselves are subject to proteasomal degradation.
