首页> 外文期刊>International Journal of Microbiology >Transcriptional Response of Selenopolypeptide Genes and Selenocysteine Biosynthesis Machinery Genes in Escherichia coli during Selenite Reduction
【24h】

Transcriptional Response of Selenopolypeptide Genes and Selenocysteine Biosynthesis Machinery Genes in Escherichia coli during Selenite Reduction

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

获取原文
获取原文并翻译 | 示例
           

摘要

Bacteria can reduce toxic selenite into less toxic, elemental selenium(Se~0), but the mechanism on how bacterial cells reduce selenite at molecular level is still not clear. We used Escherichia coli strain K12, a common bacterial strain, as a model to study its growth response to sodium selenite (Na_2SeO_3) treatment and then used quantitative real-time PCR (qRT-PCR) to quantify transcript levels of three E. coli selenopolypeptide 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 5mM Na_2SeO_3 treatment inhibited growth by ~50% while 0.001 to 0.01 mM treatments stimulated cell growth by ~30%. Under 50% inhibitory or 30% stimulatory Na_2SeO_3 concentration, selenopolypeptide genes (fdnG, fdoG, and fdhF) whose products require SeCys but not SeCys biosynthesis machinery genes were found to be induced ≥2-fold. In addition, one sulfur (S)metabolic gene iscS and two previously reported selenite-responsive genes sodA and gutS were also induced ≥2-fold under 50% inhibitory concentration. Our findings provide insight about the detoxification of selenite in E. coli via 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(Se〜0),但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(Na_2SeO_3)处理的生长反应,然后使用定量实时PCR(qRT-PCR)定量三种大肠杆菌硒多肽的转录水平硒代半胱氨酸(SeCys)生物合成和掺入多肽的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5mM Na_2SeO_3处理抑制细胞生长约50%,而0.001至0.01mM处理刺激细胞生长约30%。在抑制性Na_2SeO_3浓度为50%或30%刺激性浓度为30%的情况下,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)代谢基因iscS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倍以上。我们的发现通过诱导参与亚硒酸盐还原过程的这些基因,提供了关于在大肠杆菌中亚硒酸盐解毒的见解。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号