In a recent study published in Nature, Dr. XU Tongda's group at Shanghai Center for Plant Stress Biology of Chinese Academy of Sciences and the collaborators identified a novel auxin signaling pathway which mediate differential growth of the apical hook in Arabidopsis thaliana.

The plant phytohormone auxin plays critical roles in almost all aspects of plant development. Auxin has been repeatedly investigated to have a morphogen-like property since it acts in a concentration-dependent manner.

Apical hook formation in dicotyledonous plants is essential for protecting the shoot apical meristem from mechanical damage before the germinating seedling pushes through the soil to the surface, and it represents a classical example of a process mediated by differential auxin concentrations. However, how such auxin gradient is interpreted to mediate differential cell growth of the apical hook is still largely unexplored.

Apical hook was used in this study as the model to investigate how different concentration of auxin mediates downstream events. Researchers uncovered a novel auxin signaling mechanism.

This mechanism is triggered by auxin maximum at the concave side of the apical hook and involves auxin-mediated C-terminus cleavage and the cytosolic/nucleus translocation of Transmembrane Kinase 1 (TMK1). TMK1 C-terminus (TMK1C) then specifically interacts with and phosphorylates two non-canonical Aux/IAAs transcriptional repressors, IAA32 and IAA34 thus regulating the activity of ARF transcription factors.

In contrast to the TIR1/AFB-dependent degradation of canonical Aux/IAAs, the TMK1-dependent mechanism stabilizes the non-canonical Aux/IAAs to regulate gene expression ultimately leading to the growth inhibition.

This study provided an intriguing signaling mechanism that the plant cell transduced auxin signaling from the plasmamembrane to the nucleus through the cleavage of TMK1. It provided the evidence that the non-canonical IAAs also participate in auxin mediated plant development.

Dr. XU’s group and the collaborators are now working on how this mechanism is triggered by auxin and the underlying mechanism of the crosstalk between TIR1- and TMK- auxin signaling pathways.