The bHLH Transcription Factor bHLH104 Interacts with IAA-LEUCINE RESISTANT3 and Modulates Iron Homeostasis in Arabidopsis
The bHLH Transcription Factor bHLH104 Interacts with IAA-LEUCINE RESISTANT3 and Modulates Iron Homeostasis in Arabidopsis
复制标题
bHLH 转录因子 bHLH104 与 IAA-LEUCINE RESISTANT3 相互作用并调节拟南芥中的铁稳态
DOI：
10.1105/tpc.114.132704
复制
发表时间：
2015-03-01
期刊：
影响因子：
11.6
通讯作者：
Wang, Hong-Bin
中科院分区：
文献类型：
--
作者：
Zhang, Jie;Liu, Bing;Wang, Hong-Bin
IVc亚群bHLH转录因子bHLH 104与ILR 3相互作用，通过靶向Ib亚群bHLH基因和PYE表达调控拟南芥缺铁反应。铁是植物生长发育不可缺少的微量营养元素。植物体内铁稳态的调节是一个复杂的过程，涉及到许多转录因子。在这里，我们证明了一个基本的螺旋-环-螺旋（bHLH）转录因子，bHLH 104，属于IVc亚组的bHLH家族，作为一个关键组成部分，积极调节缺铁反应。敲除拟南芥中的bHLH 104大大降低了对铁缺乏的耐受性，而bHLH 104的过表达具有相反的效果，并导致在土壤生长条件下过量铁的积累。铁缺乏诱导基因的激活基本上受到抑制的损失bHLH 104。进一步的研究表明，bHLH 104与另一种IVc亚组bHLH蛋白质IAA-Leucine Resistant 3（ILR 3）相互作用，该蛋白质在铁稳态中也发挥重要作用。此外，bHLH 104和ILR 3可以直接结合Ib亚群bHLH基因和POPEYE（PYE）的启动子，在铁缺乏反应的调控中发挥作用。有趣的是，遗传分析表明，bHLH 104的损失可以降低由BRUTUS病变所赋予的对Fe缺乏的耐受性，BRUTUS编码E3连接酶并与bHLH 104相互作用。总的来说，我们的数据支持bHLH 104和ILR 3通过靶向Ib亚组bHLH基因和PYE表达在铁缺乏反应的调节中发挥关键作用。
The IVc subgroup bHLH transcription factor bHLH104 interacts with ILR3 to regulate the Arabidopsis Fe deficiency responses via targeting the Ib subgroup bHLH genes and PYE expression. Iron (Fe) is an indispensable micronutrient for plant growth and development. The regulation of Fe homeostasis in plants is complex and involves a number of transcription factors. Here, we demonstrate that a basic helix-loop-helix (bHLH) transcription factor, bHLH104, belonging to the IVc subgroup of bHLH family, acts as a key component positively regulating Fe deficiency responses. Knockout of bHLH104 in Arabidopsis thaliana greatly reduced tolerance to Fe deficiency, whereas overexpression of bHLH104 had the opposite effect and led to accumulation of excess Fe in soil-grown conditions. The activation of Fe deficiency-inducible genes was substantially suppressed by loss of bHLH104. Further investigation showed that bHLH104 interacted with another IVc subgroup bHLH protein, IAA-LEUCINE RESISTANT3 (ILR3), which also plays an important role in Fe homeostasis. Moreover, bHLH104 and ILR3 could bind directly to the promoters of Ib subgroup bHLH genes and POPEYE (PYE) functioning in the regulation of Fe deficiency responses. Interestingly, genetic analysis showed that loss of bHLH104 could decrease the tolerance to Fe deficiency conferred by the lesion of BRUTUS, which encodes an E3 ligase and interacts with bHLH104. Collectively, our data support that bHLH104 and ILR3 play pivotal roles in the regulation of Fe deficiency responses via targeting Ib subgroup bHLH genes and PYE expression.