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 SCF, 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.

At high vegetation density, shade-intolerant plants sense a reduction in the red (660 nm) to far-red (730 nm) light ratio (R/FR) in addition to a general reduction in light intensity. These light signals trigger a spectrum of morphological changes manifested by growth of stem-like tissue (hypocotyl, petiole, etc.) instead of harvestable organs (leaves, fruits, seeds, etc.)—namely, shade avoidance syndrome (SAS). Common phenotypical changes related to SAS are changes in leaf hyponasty, an increase in hypocotyl and internode elongation and extended petioles. Prolonged shade exposure leads to early flowering, less branching, increased susceptibility to insect herbivory, and decreased seed yield. Thus, shade avoidance significantly impacts on agronomic traits. Many genetic and molecular studies have revealed that phytochromes, cryptochromes and UVR8 (UV-B photoreceptor protein) monitor the changes in light intensity under shade and regulate the stability or activity of phytochrome-interacting factors (PIFs). PIF-governed modulation of the expression of auxin biosynthesis, transporter and signaling genes is the major driver for shade-induced hypocotyl elongation. Besides auxin, gibberellins, brassinosteroids, and ethylene are also required for shade-induced hypocotyl or petiole elongation growth. In leaves, accumulated auxin stimulates cytokinin oxidase expression to break down cytokinins and inhibit leaf growth. In the young buds, shade light promotes the accumulation of abscisic acid to repress branching. Shade light also represses jasmonate- and salicylic acid-induced defense responses to balance resource allocation between growth and defense. Here we will summarize recent findings relating to such hormonal regulation in SAS in Arabidopsis thaliana, Brassica rapa, and certain crops.

Shade avoidance syndrome enables shaded plants to grow and compete effectively against their neighbors. In Arabidopsis, the shade-induced de-phosphorylation of the transcription factor PIF7 (PHYTOCHROME-INTERACTING FACTOR 7) is the key event linking light perception to stem elongation. However, the mechanism through which phosphorylation regulates the activity of PIF7 is unclear. Here, we show that shade light induces the de-phosphorylation and nuclear accumulation of PIF7. Phosphorylation-resistant site mutations in PIF7 result in increased nuclear localization and shade-induced gene expression, and consequently augment hypocotyl elongation. PIF7 interacts with 14-3-3 proteins. Blocking the interaction between PIF7 and 14-3-3 proteins or reducing the expression of 14-3-3 proteins accelerates shade-induced nuclear localization and de-phosphorylation of PIF7, and enhances the shade phenotype. By contrast, the 14-3-3 overexpressing line displays an attenuated shade phenotype. These studies demonstrate a phosphorylation-dependent translocation of PIF7 when plants are in shade and a novel mechanism involving 14-3-3 proteins, mediated by the retention of PIF7 in the cytoplasm that suppresses the shade response.

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SummaryLight filtered through dense planting initiates the shade avoidance syndrome (SAS) in plants, which helps them compete against their neighbors. Quantitative trait loci (QTL)-based analysis identified the nighttime-expressed clock component ELF3 as a new player in the SAS, but its detailed mechanism is unclear. Here, we show that the circadian clock gates shade-induced gene expression and hypocotyl elongation at night. ELF3 is involved in nighttime suppression via interaction with and inactivation of PHYTOCHROME-INTERACTING FACTOR 7 (PIF7). Loss of function of ELF3 restores the shade induction, which is largely reduced in the absence of PIF7, indicating that ELF3 acts upstream of PIF7. Finally, we found that the repressive activity of ELF3 on the shade response is stronger under short days than under long days. Our results reveal that the interaction between ELF3 and PIF7 mediates the circadian gating of the SAS, which coordinates the daily control of physiological outputs.