Regulatory links between iron metabolism and oxidative stress in Rhodobacter sphaeroides

随着地球上氧气的出现，活性氧的出现，铁的有效性急剧下降。铁通过在芬顿反应中产生羟基自由基而增强氧毒性。因此，在氧存在下的生命需要严格调节铁代谢及其与氧化应激防御调节的耦合。铁硫簇也是重要的蛋白质氧化还原敏感元件。我们以前的工作揭示了氧化应激与类球红细菌铁代谢的许多联系。因此，我们希望使用这个已建立的光养模式生物，以进一步阐明铁代谢的α-变形杆菌的调节和它的联系，氧化应激防御。我们将确定影响铁代谢基因表达的调节因子，以应对氧化应激和铁限制或过量。同时，我们将研究已知或预测的铁和氧化还原调节剂在这些反应中的作用。野生型中mRNA水平和蛋白质合成速率的现有数据将通过突变株研究和体外研究进行补充，以阐明单个蛋白质和调节RNA的调节机制。R. sphaeroides允许区分铁的直接影响和氧化应激引起的次要影响，并分析光合复合物的影响。因此，这些研究将为细菌铁代谢和氧化应激防御的共同调节提供新的见解。

With the appearance of oxygen on earth reactive oxygen species appeared and iron availability was drastically decreased. Iron potentiates oxygen toxicity by the production of hydroxyl radicals in the Fenton reaction. Thus life in the presence of oxygen requires a strict regulation of iron metabolism and its coupling with regulation of the oxidative stress defense. Iron-sulfur clusters are also important redox-sensing elements of proteins. Our previous work revealed many links of oxidative stress to iron metabolism in Rhodobacter sphaeroides. Therefore we want to use this established phototrophic model organism to further elucidate the regulation of iron metabolism in an alpha proteobacterium and its link to the oxidative stress defense. We will identify regulatory factors that affect expression of genes for iron metabolism in response to oxidative stress and iron limitation or excess. In parallel we will investigate the role of known or predicted iron and redox regulators in these responses. The available data on mRNA levels and protein synthesis rates in the wild type will be complemented by studies in mutant strains and by in vitro studies in order to elucidate the mechanisms of regulation by the individual proteins and regulatory RNAs. The metabolic versatility of R. sphaeroides allows to discriminate between direct effects of iron and secondary effects caused by oxidative stress and to analyze the impact of photosynthetic complexes. These studies will thus provide new insights into the co-regulation of iron metabolism and oxidative stress defense in bacteria.