Phytochrome A Negatively Regulates the Shade Avoidance Response by Increasing Auxin/Indole Acidic Acid Protein Stability

• Published in: Developmental cell 2018-01, Vol.44 (1), p.29-41.e4
• Main Authors: Yang, Chuanwei, Xie, Famin, Jiang, Yupei, Li, Zhen, Huang, Xu, Li, Lin
• Format: Article
• Language: English
• Subjects: AUX/IAA; auxin signaling; phytochrome A; protein stability; shade avoidance response
• ISSN: 1534-5807; 1878-1551
• DOI: 10.1016/j.devcel.2017.11.017

The reduction in the red to far-red light ratio (R/FR) and photosynthetically active radiation caused by dense planting initiates shade avoidance responses (SARs) to help plants compete against their neighbors. However, deep shade attenuates shade-induced stem elongation to suppress excessive reversion toward skotomorphogenic development, in which photoreceptor phytochrome A (PHYA) has been known to play the major role. However, the molecular mechanism underlying PHYA function in deep shade is poorly understood. Here, we report that shade-accumulated PHYA can release auxin/indole-3-acetic acid (AUX/IAA), suppressors in the auxin signaling pathway, from SCFTIR1, an auxin receptor, to weaken auxin signaling and negatively regulate shade response. Corroborating this, phyA mutants display an enhanced auxin response to deep shade and auxin treatment. Specifically, PHYA competes with TIR1 by directly binding and stabilizing AUX/IAA. Our findings illustrate a mechanistic model of how plants sense different shade levels to fine-tune auxin signaling and generate appropriate SAR. •Photoreceptor PHYA accumulates under shade•PHYA negatively regulates auxin signal transduction•PHYA prevents degradation of AUX/IAA by competing with TIR1•PHYA-AUX/IAA interactions fine-tune shade avoidance responses Light filtered through dense planting initiates a shade avoidance response (SAR) in plants that helps them compete with their neighbors. Yang et al. now show that accumulation of photoreceptor PHYA in shaded plants prevents excessive SAR by stabilizing the auxin signaling repressors AUX/IAA through direct interaction.