当前位置 :首页>研究报道

无抗生素养鸡场的抗生素抗性基因

发布者:抗性基因网 时间:2021-06-15 浏览量:1005

  摘要

  抗生素抗性基因 (ARG) 是新兴的微污染物,对环境和人类构成潜在威胁。来自废水的污泥是 ARG 的重要来源,目前的研究主要集中在它们在微生物基因组中的存在。然而,尽管 ARG 表达仍然是功能活动的更好代表,但对表达哪些 ARG 知之甚少。本研究通过高通量定量 PCR(296 组引物)结合转录分析对污水污泥中表达的 ARGs 进行表征。共检测到 202 个 ARG 转录本,其丰度范围为 3.1 × 109 至 1.2 × 1010 拷贝/克干重。五个最丰富的 ARG 转录本(qacEdelta1-02、sul2、qacEdelta1-01、aadA2-03、tetX)的总丰度与 ARG 转录本的总丰度呈线性相关(R2 = 0.88,p < 10−4),表明这些基因可以作为定量预测表达的 ARGs 总丰度的指标。观察到表达的 ARG 的动态在夏季和冬季的丰度低于其他季节(p < 0.05,Kruskal-Wallis 检验)。变异分区分析表明,由环境属性变化引起的细菌群落结构的变化可能是表达 ARG 动态的主要驱动因素。这项研究的结果为污水污泥中的 ARG 提供了新的见解。

   Antibiotic resistance genes (ARGs) are emerging micro-pollutants that pose potential threats to environments and humans. Sewage sludge from wastewater is an important source for ARGs and current studies mainly focus on their existence in microbial genomes. However, little is known about which ARGs are expressed even though ARGs expression remains a better proxy for functional activity. In this study, the expressed ARGs in sewage sludge were characterized by high-throughput quantitative PCR (296 primer sets) combined with transcriptional analysis. A total of 202 ARG transcripts were detected and their abundances ranged from 3.1 × 109 to 1.2 × 1010 copies/g dry weight. The sum abundance of five most abundant ARG transcripts (qacEdelta1-02, sul2, qacEdelta1-01, aadA2-03, tetX) exhibited a linear correlation with the total abundance of ARG transcripts (R2 = 0.88, p < 10−4), suggesting that these genes could be regarded as indicators to quantitatively predict the total abundance of expressed ARGs. Dynamics of expressed ARGs were observed with lower abundances in summer and winter than those in other seasons (p < 0.05, Kruskal-Wallis test). Variation partitioning analysis indicated that the shift in bacterial community structures induced by changes in environmental attributes might be the main driver for the dynamics of expressed ARGs. Results of this study provided new insights into the ARGs in sewage sludge.


  cndns.com/members/signin.aspx?rtn=/userhome/index.aspx