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

Min Cao, Rong Chen, Pan Li, Yongqiang Yu, Rui Zheng, Danfeng Ge, Wei Zheng, Xuhui Wang, Yangtao Gu, Zuzana Gelová, Jiří Friml, Heng Zhang, Renyi Liu, Jun He and Tongda Xu ()
Additional contact information
Min Cao: Chinese Academy of Sciences
Rong Chen: Chinese Academy of Sciences
Pan Li: Chinese Academy of Sciences
Yongqiang Yu: Chinese Academy of Sciences
Rui Zheng: Chinese Academy of Sciences
Danfeng Ge: Chinese Academy of Sciences
Wei Zheng: Fujian Agriculture and Forestry University
Xuhui Wang: Fujian Agriculture and Forestry University
Yangtao Gu: Fujian Agriculture and Forestry University
Zuzana Gelová: Institute of Science and Technology Austria
Jiří Friml: Institute of Science and Technology Austria
Heng Zhang: Chinese Academy of Sciences
Renyi Liu: Fujian Agriculture and Forestry University
Jun He: Chinese Academy of Sciences
Tongda Xu: Fujian Agriculture and Forestry University

Nature, 2019, vol. 568, issue 7751, 240-243

Abstract: Abstract 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)1,2, 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.

Date: 2019
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DOI: 10.1038/s41586-019-1069-7

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