Iron is an essential element for plants. Iron uptake by plants is highly regulated, but the underlying mechanism is poorly understood. Using a truncated fragment of the iron deficiency-responsive bHLH100 gene promoter, we screened the Arabidopsis transcription factor yeast one-hybrid (Y1H) library and identified the DOF family protein, OBP3, as a crucial component of the iron deficiency-signaling pathway. OBP3 is a transcriptional repressor with a C-terminal activation domain. Its expression is induced by iron deficiency. The transgenic lines that overexpress OBP3 exhibited iron overload and premature leaf necrosis, while the obp3 mutant was less tolerant of iron deficiency. It was discovered that OBP3 directly targets the Ib subgroup of bHLH gene promoters. OBP3 interacts with the bHLH transcription factor ILR3 (IAA-LEUCINE RESISTANT3), and their interaction enhances the DNA-binding ability and transcriptional promoting activity of OBP3, resulting in the positive regulation of iron deficiency-response genes. In addition, the E3 Ligase BRUTUS facilitates 26S proteasome-mediated degradation of OBP3 protein to prevent excessive iron uptake in plants. In conclusion, our research emphasizes the vital role of OBP3 in regulating plant iron homeostasis.

中文翻译：

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转录因子 Dof3.6/OBP3 调节拟南芥中的铁稳态。


铁是植物的必需元素。植物对铁的吸收受到高度调节，但其潜在机制知之甚少。使用缺铁反应性 bHLH100 基因启动子的截短片段，我们筛选了拟南芥转录因子酵母单杂交 （Y1H） 文库，并鉴定了 DOF 家族蛋白 OBP3 作为缺铁信号通路的关键组成部分。OBP3 是一种具有 C 端激活结构域的转录阻遏蛋白。它的表达是由缺铁诱导的。过表达 OBP3 的转基因品系表现出铁过载和叶片过早坏死，而 OBP3 突变体对铁缺乏的耐受性较低。研究发现 OBP3 直接靶向 bHLH 基因启动子的 Ib 亚群。OBP3 与 bHLH 转录因子 ILR3 （IAA-LEUCINE RESISTANT3） 相互作用，它们的相互作用增强了 OBP3 的 DNA 结合能力和转录促进活性，导致缺铁反应基因的正调控。此外，E3 连接酶 BRUTUS 促进 OBP3 蛋白的 26S 蛋白酶体介导的降解，以防止植物过度吸收铁。总之，我们的研究强调了 OBP3 在调节植物铁稳态中的重要作用。