4.7 Article

Organ-specific COP1 control of BES1 stability adjusts plant growth patterns under shade or warmth

期刊

DEVELOPMENTAL CELL
卷 57, 期 16, 页码 2009-+

出版社

CELL PRESS
DOI: 10.1016/j.devcel.2022.07.003

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资金

  1. University of Buenos Aires [20020170100505BA]
  2. Agencia Nacional de Promocion Cientifica y Tecnologica [PICT-2019-2019-01354, PICT-2019-2019-2252, PICT2016-2234]
  3. European Regional Development Fund Project Centre for Experimental Plant Biology'' [CZ.02.1.01/0.0/0.0/16_019/0000738]
  4. National Research Foundation of Korea [2018R1A3B1052617]
  5. Spanish Ministry of Science and Innovation [PID2019109925GB-I00]
  6. Generalitat Valenciana [PROMETEO/2019/021]
  7. Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) [CEPLASEXC-2048, 390686111, IRTG 1525, GRK 2466]
  8. National Research Foundation of Korea [2018R1A3B1052617] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Under shade or warmth conditions, cotyledon cell expansion is inhibited and hypocotyl growth is promoted in Arabidopsis thaliana. The activity of the BES1 transcription factor is regulated through transcriptional and post-translational mechanisms, resulting in the repression of cotyledon cell expansion.
Under adverse conditions such as shade or elevated temperatures, cotyledon expansion is reduced and hy-pocotyl growth is promoted to optimize plant architecture. The mechanisms underlying the repression of cotyledon cell expansion remain unknown. Here, we report that the nuclear abundance of the BES1 transcrip-tion factor decreased in the cotyledons and increased in the hypocotyl in Arabidopsis thaliana under shade or warmth. Brassinosteroid levels did not follow the same trend. PIF4 and COP1 increased their nuclear abun-dance in both organs under shade or warmth. PIF4 directly bound the BES1 promoter to enhance its activity but indirectly reduced BES1 expression. COP1 physically interacted with the BES1 protein, promoting its proteasome degradation in the cotyledons. COP1 had the opposite effect in the hypocotyl, demonstrating organ-specific regulatory networks. Our work indicates that shade or warmth reduces BES1 activity by tran-scriptional and post-translational regulation to inhibit cotyledon cell expansion.

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