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肺炎链球菌D39在钴存在下的转录组分析

Transcriptome analysis of Streptococcus pneumoniae D39 in the presence of cobalt.

作者信息

Manzoor Irfan, Shafeeq Sulman, Kuipers Oscar P

机构信息

Department of Molecular Genetics, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Nijenborgh 7, 9747 AG Groningen, The Netherlands ; Department of Bioinformatics and Biotechnology, Government College University, Faisalabad, Pakistan.

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Nobels väg 16, 17177 Stockholm, Sweden.

出版信息

Genom Data. 2015 Sep 8;6:151-3. doi: 10.1016/j.gdata.2015.08.033. eCollection 2015 Dec.

Abstract

Cobalt (Co(2 +)) is an important transition metal ion that plays a vital role in cellular physiology of bacteria. The role of Co(2 +) in the regulation of several genes/operons in Streptococcus pneumoniae has recently been reported [1]. The data described in this article relate to the genome-wide transcriptional profiling of Streptococcus pneumoniae D39, either in the presence or absence of 0.5 mM Co(2 +) in chemically defined medium (CDM) using DNA microarray analysis. Genes belonging to a broad range of cellular processes such as virulence, transport and efflux systems, stress response and surface attachment were differentially expressed in the presence of Co(2 +). We used transcriptional lacZ assays and electrophoretic mobility shift assays (EMSAs) to confirm our results [1]. The dataset is publicly available at the Gene Expression Omnibus (GEO) repository (http://www.ncbi.nlm.nih.gov/geo/) with accession number GSE57696.

摘要

钴(Co(2+))是一种重要的过渡金属离子,在细菌的细胞生理学中起着至关重要的作用。最近有报道称Co(2+)在肺炎链球菌中对多个基因/操纵子的调控作用[1]。本文所述数据涉及在化学限定培养基(CDM)中,存在或不存在0.5 mM Co(2+)的情况下,使用DNA微阵列分析对肺炎链球菌D39进行全基因组转录谱分析。属于广泛细胞过程(如毒力、转运和外排系统、应激反应和表面附着)的基因在Co(2+)存在时差异表达。我们使用转录lacZ分析和电泳迁移率变动分析(EMSA)来证实我们的结果[1]。该数据集可在基因表达综合数据库(GEO)存储库(http://www.ncbi.nlm.nih.gov/geo/)中公开获取,登录号为GSE57696。

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Genome of the bacterium Streptococcus pneumoniae strain R6.肺炎链球菌R6菌株的基因组。
J Bacteriol. 2001 Oct;183(19):5709-17. doi: 10.1128/JB.183.19.5709-5717.2001.

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