Two bHLH Transcription Factors, bHLH34 and bHLH104, Regulate Iron Homeostasis in Arabidopsis thaliana

Two bHLH Transcription Factors, bHLH34 and bHLH104, Regulate Iron Homeostasis in Arabidopsis thaliana
复制标题

DOI:
10.1104/pp.15.01827
复制
发表时间:
2016-04-01
期刊:
影响因子:
7.4
通讯作者:
Yu, Diqiu
Yu, Diqiu
中科院分区:
生物学1区
文献类型:
--
作者:
Li, Xiaoli;Zhang, Huimin;Yu, Diqiu

文献摘要

被引文献

相似文献

铁(Fe)动态平衡的调节对植物的生存至关重要。尽管植物体内铁的还原、吸收和转运系统已经被描述,但植物感知铁状态和协调铁缺乏反应基因表达的分子机制还很不清楚。在此,我们报道了两个基本的螺旋-环-螺旋型转录因子bHLH34和bHLH104正向调节拟南芥(Arabitopsis Thaliana)的铁稳态。BHLH34和bHLH104功能的丧失会导致铁缺乏反应的中断和铁含量的减少,而过表达植物则结构性地促进铁缺乏反应基因的表达和铁的积累。进一步分析表明,bHLH34和bHLH104直接激活了Ib亚群bHLH基因bHLH38/39/100/101的转录。此外,bHLH101的过表达部分挽救了bhlh34bhlh104双突变体的缺铁表型。进一步的研究表明,bHLH34、bHLH104和bHLH105(IAA-亮氨酸RESISTANT3)作为同源或异源二聚体发挥着非冗余调节铁稳态的作用。这项工作揭示了植物已经进化出复杂的分子机制来调节缺铁反应基因以适应缺铁条件。
The regulation of iron (Fe) homeostasis is critical for plant survival. Although the systems responsible for the reduction, uptake, and translocation of Fe have been described, the molecular mechanism by which plants sense Fe status and coordinate the expression of Fe deficiency-responsive genes is largely unknown. Here, we report that two basic helix-loop-helix-type transcription factors, bHLH34 and bHLH104, positively regulate Fe homeostasis in Arabidopsis (Arabidopsis thaliana). Loss of function of bHLH34 and bHLH104 causes disruption of the Fe deficiency response and the reduction of Fe content, whereas overexpression plants constitutively promote the expression of Fe deficiency-responsive genes and Fe accumulation. Further analysis indicates that bHLH34 and bHLH104 directly activate the transcription of the Ib subgroup bHLH genes, bHLH38/39/100/101. Moreover, overexpression of bHLH101 partially rescues the Fe deficiency phenotypes of bhlh34bhlh104 double mutants. Further investigation suggests that bHLH34, bHLH104, and bHLH105 (IAA-LEUCINE RESISTANT3) function as homodimers or heterodimers to nonredundantly regulate Fe homeostasis. This work reveals that plants have evolved complex molecular mechanisms to regulate Fe deficiency response genes to adapt to Fe deficiency conditions.