转录因子MYB30通过维持FIT转录因子的稳定性来促进铁稳态

Hongyun Zhao, Juntao Jiang, Mengai Shen, Yiyi Zhang, Yamei Zhang, Huilin Liu, Huapeng Zhou, Yuan Zheng
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引用次数: 0

摘要

铁(Fe)是植物生长发育的重要营养物质。在拟南芥(Arabidopsis thaliana)中,bHLH转录因子FER-LIKE IRON DEFICIENCY INDUCED transcription factor (FIT)在调节铁缺乏反应中起关键作用。我们的研究表明,R2R3-MYB转录因子MYB30是通过调节FIT稳定性来调节铁缺乏反应的正调节因子。MYB30功能缺失突变的植物表现出明显的缺铁症状和铁吸收减少,而MYB30过表达导致相反的效果。我们发现MYB30与BRUTUS LIKE1 (BTSL1)和BTSL2相互作用,这两个部分冗余的E3泛素连接酶负调控铁缺乏反应。MYB30通过其MYB dna结合域与BTSL1的c端区域结合,从而保护FIT免受BTSL1介导的泛素化和降解,导致FIT积累以应对缺铁反应。综上所述,我们的研究揭示了转录因子MYB30作为FIT稳定性的调节因子的作用,它反过来调节植物对铁缺乏的铁稳态。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The transcription factor MYB30 promotes iron homeostasis by maintaining the stability of the FIT transcription factor
Iron (Fe) is a vital nutrient for the growth and development of plants. In Arabidopsis (Arabidopsis thaliana), the bHLH transcription factor FER-LIKE IRON DEFICIENCY INDUCED TRANSCRIPTION FACTOR (FIT) plays a pivotal role in regulating the response to Fe deficiency. Our study reveals that the R2R3-MYB transcription factor MYB30 is a positive regulator of the Fe-deficiency response by regulating FIT stability. Plants with loss-of-function mutations in MYB30 exhibit pronounced Fe-deficiency symptoms and diminished Fe uptake, while overexpression of MYB30 leads to the opposite effects. We have discovered that MYB30 interacts with BRUTUS LIKE1 (BTSL1) and BTSL2, two partially redundant E3 ubiquitin ligases that negatively regulate the Fe-deficiency response. MYB30 binds to the C-terminal region of BTSL1 through its MYB DNA-binding domain, thereby safeguarding FIT from BTSL1-mediated ubiquitination and degradation, resulting in FIT accumulation for Fe deficiency response. In summary, our research uncovers the role of the transcription factor MYB30 as a regulator of FIT stability, which in turn modulates Fe homeostasis in plants in response to Fe deficiency.
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