非TIR1受体依赖型激活生长素信号的新机制  

A TIR1-independent Auxin Signaling Module

作　　者：胡孔琴 丁兆军[1] Hu Kongqin;Ding Zhaojun(Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, College of Life Sciences, Shandong University, Qingdao 266237, China)

机构地区：[1]山东大学生命科学学院植物发育与环境适应教育部重点实验室,青岛266237

出　　处：《植物学报》2019年第3期293-295,共3页Chinese Bulletin of Botany

摘　　要：依赖于受体TIR1以及下游Aux/IAAs-ARFs介导的信号通路是目前研究最为深入的生长素信号转导途径。徐通达课题组最新研究发现,高浓度生长素能够诱导质膜定位的TMK1激酶发生剪切,导致其羧基(C-)端部分转入细胞核并磷酸化修饰细胞核内的非经典IAA32/34,后者通过与生长素响应转录因子ARFs互作,调控下游基因表达,从而解析了生长素通过TMK1-IAA32/34-ARFs通路调控植物顶端弯钩内外侧差异性生长的分子机制。该研究发现了一条新的生长素TMK1-IAA32/34-ARFs信号途径,此信号通路独立于经典生长素受体TIR1介导的生长素信号转导通路。The most well established auxin signaling pathway is initiated from transport inhibitor response (TIR1)-mediated perception and degradation of Aux/IAAs, eventually leads to depression of auxin response factors (ARFs). A recent study from the Tongda Xu lab showed that high levels of auxin induced the cleavage of the plasma membrane localized transmembrane kinase receptor 1 (TMK1). The cleaved TMK1 C-terminus translocated to the nucleus and phosphorylated the nuclear localized non-canonical IAA32/34, which regulate the auxin signaling response by interacting with ARFs. The TMK1-IAA32/34-ARFs module, acting independently from the TIR1-dependent auxin signaling pathway, nicely interprets how the local auxin accumulation modulates asymmetric growth during apical hook development.

关 键 词：生长素 信号转导 TMK1 

分 类 号：Q945[生物学—植物学]