Control of Fur synthesis by the non-coding RNA RyhB and iron-responsive decoding
Control of Fur synthesis by the non-coding RNA RyhB and iron-responsive decoding
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DOI：
10.1038/sj.emboj.7601553
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发表时间：
2007-02-21
期刊：
影响因子：
11.4
通讯作者：
Blaesi, Udo
中科院分区：
文献类型：
--
作者：
Vecerek, Branislav;Moll, Isabella;Blaesi, Udo
Fe 2+依赖性Fur蛋白是细菌铁吸收的负调节因子。由于只有金属-Fur作为一种自生抑制物，当不明显需要持续供应时，Fe 2+的缺乏将指导Fur的表达。我们表明，在大肠杆菌中的转录后调控机制，确保毛皮合成保持稳定的铁限制。我们的研究表明，毛皮翻译耦合到上游开放阅读框架（uof），其翻译下调的非编码RNA（ncRNA）RyhB。由于RyhB转录受金属-Fur负控制，铁消耗产生负反馈回路。RyhB介导的uof-fur调节提供了通过反式编码的ncRNA进行间接翻译调节的第一个实例。此外，我们提出的证据，铁响应解码机制的uof-fur实体。它可以作为RyhB电路的备用机制，代表铁的可用性和含铁蛋白质合成之间的第一个联系。
The Fe2+-dependent Fur protein serves as a negative regulator of iron uptake in bacteria. As only metallo-Fur acts as an autogeneous repressor, Fe2+ scarcity would direct fur expression when continued supply is not obviously required. We show that in Escherichia coli post-transcriptional regulatory mechanisms ensure that Fur synthesis remains steady in iron limitation. Our studies revealed that fur translation is coupled to that of an upstream open reading frame (uof), translation of which is downregulated by the non-coding RNA (ncRNA) RyhB. As RyhB transcription is negatively controlled by metallo-Fur, iron depletion creates a negative feedback loop. RyhB-mediated regulation of uof-fur provides the first example for indirect translational regulation by a trans-encoded ncRNA. In addition, we present evidence for an iron-responsive decoding mechanism of the uof-fur entity. It could serve as a backup mechanism of the RyhB circuitry, and represents the first link between iron availability and synthesis of an iron-containing protein.