非TIR1受体依赖型激活生长素信号的新机制

doi:10.11983/CBB19063

植物学报 ›› 2019, Vol. 54 ›› Issue (3): 293-295.DOI: 10.11983/CBB19063

非TIR1受体依赖型激活生长素信号的新机制

胡孔琴,丁兆军()

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

收稿日期:2019-03-29 接受日期:2019-03-31 出版日期:2019-07-01 发布日期:2019-05-20
通讯作者: 丁兆军

A TIR1-independent Auxin Signaling Module

Kongqin Hu,Zhaojun Ding()

Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, College of Life Sciences, Shandong University, Qingdao 266237, China

Received:2019-03-29 Accepted:2019-03-31 Online:2019-07-01 Published:2019-05-20
Contact: Zhaojun Ding

摘要/Abstract

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。

关键词: 生长素, 信号转导, TMK1

Abstract: 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.

Key words: auxin, signal transduction, TMK1

胡孔琴,丁兆军. 非TIR1受体依赖型激活生长素信号的新机制. 植物学报, 2019, 54(3): 293-295.

Kongqin Hu,Zhaojun Ding. A TIR1-independent Auxin Signaling Module. Chinese Bulletin of Botany, 2019, 54(3): 293-295.

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链接本文: https://www.chinbullbotany.com/CN/10.11983/CBB19063

https://www.chinbullbotany.com/CN/Y2019/V54/I3/293

图/表 1

图1 生长素信号转导途径低浓度生长素主要通过受体TIR1泛素化并降解经典的Aux/IAAs蛋白, 解除对生长素响应因子ARFs的抑制, 启动对下游基因的调控及生长素信号响应。高浓度生长素主要通过TMK1蛋白激酶磷酸化并稳定非经典Aux/IAA32/34, 抑制ARFs的活性。TMK1-IAA32/34-ARFs模型解释了植物发育过程中生长素积累调控顶端弯钩内外侧的差异性生长。

Figure 1 Pathway of auxin signal transduction The perception of low levels of auxin is mainly mediated through the TIR1 receptor, which ubiquitinates and degrades Aux/IAAs proteins, and thus de-represses ARFs to activate downstream gene transcription and trigger auxin responses. Higher levels of auxin activate TMK1, which phosphorylates and stabilizes non-canonical IAA32/34, and repress ARFs activities. The TMK1-IAA32/34-ARFs module interprets how the local auxin accumulation modulates asymmetric growth during apical hook development.

参考文献 10

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非TIR1受体依赖型激活生长素信号的新机制

A TIR1-independent Auxin Signaling Module

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