首页> 外文期刊>International Journal of Microbiology >Transcriptional Response of Selenopolypeptide Genes and Selenocysteine Biosynthesis Machinery Genes inEscherichia coliduring Selenite Reduction
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Transcriptional Response of Selenopolypeptide Genes and Selenocysteine Biosynthesis Machinery Genes inEscherichia coliduring Selenite Reduction

机译:亚硒酸盐还原过程中大肠杆菌中硒多肽基因和硒代半胱氨酸生物合成机制基因的转录响应

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Bacteria can reduce toxic selenite into less toxic, elemental selenium (Se0), but the mechanism on how bacterial cells reduce selenite at molecular level is still not clear. We usedEscherichia colistrain K12, a common bacterial strain, as a model to study its growth response to sodium selenite (Na2SeO3) treatment and then used quantitative real-time PCR (qRT-PCR) to quantify transcript levels of threeE. coliselenopolypeptide genes and a set of machinery genes for selenocysteine (SeCys) biosynthesis and incorporation into polypeptides, whose involvements in the selenite reduction are largely unknown. We determined that 5 mM Na2SeO3treatment inhibited growth by∼50% while 0.001 to 0.01 mM treatments stimulated cell growth by∼30%. Under 50% inhibitory or 30% stimulatory Na2SeO3concentration, selenopolypeptide genes (fdnG,fdoG, andfdhF) whose products require SeCys but not SeCys biosynthesis machinery genes were found to be induced ≥2-fold. In addition, one sulfur (S) metabolic geneiscSand two previously reported selenite-responsive genessodAandgutSwere also induced ≥2-fold under 50% inhibitory concentration. Our findings provide insight about the detoxification of selenite inE. colivia induction of these genes involved in the selenite reduction process.
机译:细菌可以将有毒的亚硒酸盐还原成毒性较小的元素硒(Se0),但是细菌细胞如何在分子水平上还原亚硒酸盐的机制仍不清楚。我们使用大肠杆菌菌株K12(一种常见的细菌菌株)作为模型来研究其对亚硒酸钠(Na2SeO3)处理的生长反应,然后使用实时定量PCR(qRT-PCR)来定量3E的转录水平。硒代半胱氨酸(SeCys)生物合成和掺入多肽的大肠菌硒多肽基因和一组机器基因,其参与亚硒酸盐还原的作用在很大程度上是未知的。我们确定5 mM Na2SeO3处理抑制细胞生长约50%,而0.001至0.01 tomM处理刺激细胞生长约30%。在50%抑制性Na2SeO3浓度或30%刺激性Na2SeO3浓度下,发现其产物需要SeCys而不需要SeCys生物合成机制基因的硒多肽基因(fdnG,fdoG和fdhF)被诱导≥2倍。此外,在50%抑制浓度下,一个硫(S)代谢成因和两个先前报道的亚硒酸盐响应基因sodA和GutS也被诱导了≥2倍。我们的发现提供了有关亚硒酸盐在E中解毒的见解。大肠埃希菌通过诱导这些基因参与亚硒酸盐的还原过程。

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