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Abstract：
Iron (Fe) is an important micronutrient for plant growth and development but any excess of Fe is toxic because of the Fe-dependent generation of reactive oxygen species (ROS). Thus, Fe homeostasis must be tightly regulated. In Arabidopsis thaliana, a cascade of transcription factors has been identified as involved in the regulation of this process by modulating the expression of genes related to Fe uptake, transport, and storage. Recently, it was demonstrated that in response to Fe deficiency, bHLH121/URI (UPSTREAM REGULATOR OF IRT1) directly activates the expression of several genes involved in this regulatory network. It was also shown that bHLH121 interacts with ILR3 (bHLH105) and its homologs. Herein it is shown that bHLH121 is necessary for the expression of the main markers of the plant responses to Fe excess, the ferritin genes (i.e. FER1, FER3, and FER4). bHLH121 regulates ferritin genes expression by directly binding to their promoters, at the same locus than the ILR3-PYE repressive complex. Therefore, this study highlight that bHLH121, PYE, and ILR3 form a chain of antagonistic switches that regulate the expression of ferritin genes. The implication of this finding is discussed.
摘要：
铁（Fe）是植物生长和发育的重要微量营养素，但由于Fe依赖性产生活性氧（ROS），任何过量的Fe都是有毒的。因此，铁稳态必须受到严格调控。在拟南芥中，通过调节与铁摄取相关的基因的表达，已经确定了转录因子的级联参与该过程的调节，运输,和存储。最近,研究表明，为了应对缺铁，bHLH121/URI(IRT1的上游调控器)直接激活参与该调控网络的几个基因的表达。还显示bHLH121与ILR3(bHLH105)及其同源物相互作用。本文表明，bHLH121对于植物对Fe过量反应的主要标记的表达是必需的，铁蛋白基因(即FER1、FER3和FER4)。bHLH121通过直接结合其启动子来调节铁蛋白基因的表达，在与ILR3-PYE抑制复合物相同的基因座上。因此,这项研究强调了BHLH121，PYE，和ILR3形成调节铁蛋白基因表达的拮抗开关链。讨论了这一发现的含义。
