4.8 Article

Green means go: Green light promotes hypocotyl elongation via brassinosteroid signaling

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PLANT CELL
卷 35, 期 5, 页码 1304-1317

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OXFORD UNIV PRESS INC
DOI: 10.1093/plcell/koad022

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Using a pure green light source, this study found that green light promotes hypocotyl elongation in Arabidopsis thaliana and other plants by activating the brassinosteroid signaling pathway. This discovery is important for understanding the physiological response of plants to green light and their adaptation to a green-light-dominant environment.
Although many studies have elucidated the mechanisms by which different wavelengths of light (blue, red, far-red, or ultraviolet-B [UV-B]) regulate plant development, whether and how green light regulates plant development remains largely unknown. Previous studies reported that green light participates in regulating growth and development in land plants, but these studies have reported conflicting results, likely due to technical problems. For example, commercial green light-emitting diode light sources emit a little blue or red light. Here, using a pure green light source, we determined that unlike blue, red, far-red, or UV-B light, which inhibits hypocotyl elongation, green light promotes hypocotyl elongation in Arabidopsis thaliana and several other plants during the first 2-3 d after planting. Phytochromes, cryptochromes, and other known photoreceptors do not mediate green-light-promoted hypocotyl elongation, but the brassinosteroid (BR) signaling pathway is involved in this process. Green light promotes the DNA binding activity of BRI1-EMS-SUPPRESSOR 1 (BES1), a master transcription factor of the BR pathway, thus regulating gene transcription to promote hypocotyl elongation. Our results indicate that pure green light promotes elongation via BR signaling and acts as a shade signal to enable plants to adapt their development to a green-light-dominant environment under a canopy. In contrast to blue, red, far-red or UV-B light, which inhibit hypocotyl elongation, green light promotes hypocotyl elongation via promoting brassinosteroid signaling.

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