非TIR1受体依赖型激活生长素信号的新机制

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。

A TIR1-independent Auxin Signaling Module

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.