Snapshot of iron response in Shewanella oneidensis by gene network reconstruction.
Snapshot of iron response in Shewanella oneidensis by gene network reconstruction.
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DOI：
10.1186/1471-2164-10-131
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发表时间：
2009-03-25
期刊：
影响因子：
4.4
通讯作者：
Zhou J
中科院分区：
文献类型：
--
作者：
Yang Y;Harris DP;Luo F;Xiong W;Joachimiak M;Wu L;Dehal P;Jacobsen J;Yang Z;Palumbo AV;Arkin AP;Zhou J
Shewanella oneidensis 是一种具有高铁含量的 γ-变形菌，其铁稳态受全局转录因子 Fur 的调节。然而，关于响应铁浓度变化的其他生物途径以及响应细节的知识并不完整。在这项工作中，我们整合了生理学、转录组学和遗传学方法来描述 S. oneidensis 的铁反应。我们表明 S. oneidensis 中的铁反应是一个快速过程。检查时间基因表达谱的铁消耗和补充，并重建基因共表达网络。铁获取系统、无氧能量代谢和蛋白质降解的模块是基因网络中最值得注意的。生物信息学分析表明，每个模块中的基因可能分别受到 DNA 结合蛋白 Fur、CRP 和 RpoH 的调节。对这些模块的仔细检查揭示了一个参与铁获取的转录调节因子（SO2426）和十个参与无氧能量代谢的转录因子。通过遗传学研究对网络中选定的基因进行分析。编码假定的 alcaligin 生物合成蛋白 (SO3032) 的基因和先前参与蛋白质降解的基因 (SO2017) 的破坏导致铁缺乏条件下严重的生长缺陷。一种新型转录因子（SO1415）的破坏导致硫代硫酸盐或TMAO作为电子受体的厌氧铁还原和生长缺陷，这表明SO1415是厌氧能量代谢途径的特定分支所必需的。使用重建的基因网络，我们确定了在铁耗尽和补充期间差异表达的主要生物途径。遗传学研究不仅证明了铁获取和蛋白质降解对于铁消耗的重要性，而且还鉴定了一种在无氧能量代谢中发挥作用的新型转录因子（SO1415）。
Iron homeostasis of Shewanella oneidensis, a γ-proteobacterium possessing high iron content, is regulated by a global transcription factor Fur. However, knowledge is incomplete about other biological pathways that respond to changes in iron concentration, as well as details of the responses. In this work, we integrate physiological, transcriptomics and genetic approaches to delineate the iron response of S. oneidensis. We show that the iron response in S. oneidensis is a rapid process. Temporal gene expression profiles were examined for iron depletion and repletion, and a gene co-expression network was reconstructed. Modules of iron acquisition systems, anaerobic energy metabolism and protein degradation were the most noteworthy in the gene network. Bioinformatics analyses suggested that genes in each of the modules might be regulated by DNA-binding proteins Fur, CRP and RpoH, respectively. Closer inspection of these modules revealed a transcriptional regulator (SO2426) involved in iron acquisition and ten transcriptional factors involved in anaerobic energy metabolism. Selected genes in the network were analyzed by genetic studies. Disruption of genes encoding a putative alcaligin biosynthesis protein (SO3032) and a gene previously implicated in protein degradation (SO2017) led to severe growth deficiency under iron depletion conditions. Disruption of a novel transcriptional factor (SO1415) caused deficiency in both anaerobic iron reduction and growth with thiosulfate or TMAO as an electronic acceptor, suggesting that SO1415 is required for specific branches of anaerobic energy metabolism pathways. Using a reconstructed gene network, we identified major biological pathways that were differentially expressed during iron depletion and repletion. Genetic studies not only demonstrated the importance of iron acquisition and protein degradation for iron depletion, but also characterized a novel transcriptional factor (SO1415) with a role in anaerobic energy metabolism.
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