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转录因子MYB30通过维持FIT转录因子的稳定性来促进铁稳态。

The transcription factor MYB30 promotes iron homeostasis by maintaining the stability of the FIT transcription factor.

作者信息

Zhao Hongyun, Jiang Juntao, Shen Mengai, Zhang Yiyi, Zhang Yamei, Liu Huilin, Zhou Huapeng, Zheng Yuan

机构信息

Institute of Future Agriculture, Northwest Agriculture and Forestry University, Yangling 712100, China.

State Key Laboratory of Crop Stress Adaptation and Improvement, School of Life Sciences, Henan University, Kaifeng 475004, China.

出版信息

Plant Cell. 2025 May 9;37(5). doi: 10.1093/plcell/koaf090.

Abstract

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, 2 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.

摘要

铁(Fe)是植物生长发育所必需的营养元素。在拟南芥(Arabidopsis thaliana)中,bHLH转录因子类铁缺乏诱导转录因子(FER-LIKE IRON-DEFICIENCY-INDUCED TRANSCRIPTION FACTOR,FIT)在调节对缺铁的反应中起关键作用。我们的研究表明,R2R3-MYB转录因子MYB30通过调节FIT的稳定性,是缺铁反应的正调控因子。MYB30功能缺失突变的植物表现出明显的缺铁症状,铁吸收减少,而MYB30的过表达则产生相反的效果。我们发现,MYB30与BRUTUS LIKE1(BTSL1)和BTSL2相互作用,这两个部分冗余的E3泛素连接酶对缺铁反应起负调控作用。MYB30通过其MYB DNA结合结构域与BTSL1的C末端区域结合,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。总之,我们的研究揭示了转录因子MYB30作为FIT稳定性调节因子的作用,进而在植物中调节铁稳态以应对缺铁。

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