Gibberellin regulates the Arabidopsis floral transition through miR156-targeted 
SQUAMOSA promoter binding-like transcription factors

Yu, S; Galvão, VC; Zhang, Y-C; Horrer, D; Zhang, T-Q; Hao, Y-H; Feng, Y-Q; Wang, S; Schmid, M; Wang, J-W

doi:10.1105/tpc.112.101014

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Gibberellin regulates the Arabidopsis floral transition through miR156-targeted SQUAMOSA promoter binding-like transcription factors

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Galvão, VC
Department Molecular Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Horrer, D
Department Molecular Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Schmid, M
Department Molecular Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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引用

Yu, S., Galvão, V., Zhang, Y.-C., Horrer, D., Zhang, T.-Q., Hao, Y.-H., Feng, Y.-Q., Wang, S., Schmid, M., & Wang, J.-W. (2012). Gibberellin regulates the Arabidopsis floral transition through miR156-targeted SQUAMOSA promoter binding-like transcription factors. Plant Cell, 24(8), 3320-3332. doi:10.1105/tpc.112.101014.

引用: https://hdl.handle.net/21.11116/0000-000A-B63F-3

要旨

Gibberellin (GA), a diterpene hormone, plays diverse roles in plant growth and development, including seed germination, stem elongation, and flowering time. Although it is known that GA accelerates flowering through degradation of transcription repressors, DELLAs, the underlying mechanism is poorly understood. We show here that DELLA directly binds to microRNA156 (miR156)-targeted SQUAMOSA PROMOTER BINDING-LIKE (SPL) transcription factors, which promote flowering by activating miR172 and MADS box genes. The interaction between DELLA and SPL interferes with SPL transcriptional activity and consequently delays floral transition through inactivating miR172 in leaves and MADS box genes at shoot apex under long-day conditions or through repressing MADS box genes at the shoot apex under short-day conditions. Our results elucidate the molecular mechanism by which GA controls flowering and provide the missing link between DELLA and MADS box genes.