4.8 Article

Brassinosteroid-Activated BRI1-EMS-SUPPRESSOR 1 Inhibits Flavonoid Biosynthesis and Coordinates Growth and UV-B Stress Responses in Plants

期刊

PLANT CELL
卷 32, 期 10, 页码 3224-3239

出版社

AMER SOC PLANT BIOLOGISTS
DOI: 10.1105/tpc.20.00048

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资金

  1. National Key Research and Development Program of China [2016YFD0100404]
  2. National Natural Science Foundation of China [31825004, 31721001, 31730009, 31670282, 31670307, 31470433]
  3. Strategic Priority Research Program of the Chinese Academy of Sciences [XDB27030000]
  4. Program of Shanghai Academic Research Leader
  5. National Institute of General Medical Sciences

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UV-B light is a potential stress factor in plants, but how plants coordinate growth and UV-B stress responses is not well understood. Here, we report that brassinosteroid (BR) signaling inhibits UV-B stress responses in Arabidopsis (Arabidopsis thaliana) and various crops by controlling flavonol biosynthesis. We further demonstrate that BRI1-EMS-SUPPRESSOR 1 (BES1) mediates the tradeoff between plant growth and UV-B defense responses. BES1, a master transcription factor involved in BR signaling, represses the expression of transcription factor genes MYB11, MYB12, and MYB111, which activate flavonol biosynthesis. BES1 directly binds to the promoters of these MYBs in a BR-enhanced manner to repress their expression, thereby reducing flavonol accumulation. However, exposure to broadband UV-B down-regulates BES1 expression, thus promoting flavonol accumulation. These findings demonstrate that BR-activated BES1 not only promotes growth but also inhibits flavonoid biosynthesis. UV-B stress suppresses the expression of BES1 to allocate energy to flavonoid biosynthesis and UV-B stress responses, allowing plants to switch from growth to UV-B stress responses in a timely manner. BES1, a key transcription factor involved in brassinosteroid signaling, coordinates plant growth and stress responses under ever-changing UV-B conditions by modulating flavonol biosynthesis.

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