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Brassinosteroid signalling suppresses chlorophyll biosynthesis via BGH2-GLK modules to ensure proper cotyledon greening during de-etiolation
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DOI：10.1093/pcp/pcag087.png)
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Abstract
En 中文
Brassinosteroids (BRs) are phytohormones that play essential roles in skotomorphogenesis under dark conditions, coordinating not only developmental but also plastidial regulation. Because chlorophyll precursors such as protochlorophyllide (Pchlide) can accumulate in etioplasts and generate harmful reactive oxygen species (ROS) upon light illumination, chlorophyll biosynthesis must be tightly controlled in the dark. Although BR signalling is known to repress chlorophyll biosynthesis in dark, the detailed molecular mechanisms remain unclear. Here, we identify BPG4 HOMOLOGOUS GENE 2 (BGH2) as a critical downstream component of BR signalling required for light adaptation in Arabidopsis thaliana. The BR biosynthesis-specific inhibitor, Brz, inhibited healthy cotyledon greening during de-etiolation by increasing expression of chlorophyll biosynthetic genes, and leading to excessive accumulation of Pchlide and consequent ROS-mediated cell death. Brz-induced photobleaching during de-etiolation was rescued by both overexpression of BGH2 and deficiency of the GOLDEN2-LIKE 1/2 (GLK1/2) transcription factors which control chlorophyll biosynthesis downstream of BGH2. BGH2 expression was downregulated by Brz treatment but activated by a master transcription factor of BR signalling BRZ-INSENSITIVE-LONG HYPOCOTYL 1/ BRASSINAZOLE RESISTANT 1 (BIL1/BZR1), which directly bound to the BGH2 promoter region. Knockout of BGH2 substantially suppressed the enhanced greening phenotype of bil1-D/bzr1-D, indicating that BGH2 acts as a major regulatory factor downstream of BIL1/BZR1 in regulating cotyledon greening during de-etiolation. Together, our findings suggest BGH2 as a crucial downstream component of BR signalling that fine-tunes chlorophyll biosynthesis in the dark, thereby ensuring optimal cotyledon greening during de-etiolation.
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