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Nature：TMK1介导的生长素信号调控植物的顶勾发育

已有 6614 次阅读 2019-4-11 15:10 |个人分类:每日摘要|系统分类:论文交流

TMK1-mediated auxin signalling regulates differential growth of the apical hook

First author: Min Cao; Affiliations: CAS Center for Excellence in Molecular Plant Sciences (中科院分子植物科学卓越创新中心): Shanghai, China

Corresponding author: Tongda Xu

The plant hormone auxin has crucial roles in almost all aspects of plant growth and development. Concentrations of auxin vary across different tissues, mediating distinct developmental outcomes and contributing to the functional diversity of auxin. However, the mechanisms that underlie these activities are poorly understood. Here we identify an auxin signalling mechanism, which acts in parallel to the canonical auxin pathway based on the transport inhibitor response1 (TIR1) and other auxin receptor F-box (AFB) family proteins (TIR1/AFB receptors), that translates levels of cellular auxin to mediate differential growth during apical-hook development. This signalling mechanism operates at the concave side of the apical hook, and involves auxin-mediated C-terminal cleavage of transmembrane kinase 1 (TMK1). The cytosolic and nucleus-translocated C terminus of TMK1 specifically interacts with and phosphorylates two non-canonical transcriptional repressors of the auxin or indole-3-acetic acid (Aux/IAA) family (IAA32 and IAA34), thereby regulating ARF transcription factors. In contrast to the degradation of Aux/IAA transcriptional repressors in the canonical pathway, the newly identified mechanism stabilizes the non-canonical IAA32 and IAA34 transcriptional repressors to regulate gene expression and ultimately inhibit growth. The auxin–TMK1 signalling pathway originates at the cell surface, is triggered by high levels of auxin and shares a partially overlapping set of transcription factors with the TIR1/AFB signalling pathway. This allows distinct interpretations of different concentrations of cellular auxin, and thus enables this versatile signalling molecule to mediate complex developmental outcomes.

植物激素生长素几乎在植物生长和发育的方方面面都发挥重要的作用。生长素的浓度在不同的组织间各有不同，介导不同的发育进程，作用于生长素功能的多样性。然而，这些生长素介导的发育调控潜在的分子机理还不太清楚。本文中，作者鉴定了一个生长素信号转导机制，与经典的依赖于TIR1/AFB受体的生长素通路平行发挥作用，在顶钩发育的过程中根据细胞层面的生长素水平介导差异生长。该信号机制在顶勾的凹面发挥作用，涉及到生长素介导的TMK1蛋白C端剪切。细胞质和核易位的TMK1蛋白C端特异与两个非典型生长素抑制子Aux/IAA家族的IAA32和IAA34互作，并且能够磷酸化这两个蛋白，进而调控ARF转录因子。与经典生长素信号通路中Aux/IAA转录抑制子的降解相反，作者新鉴定的机制通过稳定IAA32和IAA34这两个转录抑制子来调控基因的表达，并最终抑制生长。生长素-TMK1信号通路起始于细胞表面，受到高水平生长素的诱导，并且与TIR1/AFB信号通路共享某些转录因子。