Manzoor Irfan, Shafeeq Sulman, Afzal Muhammad, Kuipers Oscar P
Department of Molecular Genetics, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen Groningen, Netherlands ; Department of Bioinformatics and Biotechnology, Government College University Faisalabad Faisalabad, Pakistan.
Department of Molecular Genetics, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen Groningen, Netherlands ; Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet Stockholm, Sweden.
Front Cell Infect Microbiol. 2015 Dec 8;5:91. doi: 10.3389/fcimb.2015.00091. eCollection 2015.
By using a transcriptomic approach, we have elucidated the effect of Ni(2+) on the global gene expression of S. pneumoniae D39 by identifying several differentially expressed genes/operons in the presence of a high extracellular concentration of Ni(2+). The genes belonging to the AdcR regulon (adcRCBA, adcAII-phtD, phtA, phtB, and phtE) and the PsaR regulon (pcpA, prtA, and psaBCA) were highly upregulated in the presence of Ni(2+). We have further studied the role of Ni(2+) in the regulation of the AdcR regulon by using ICP-MS analysis, electrophoretic mobility shift assays and transcriptional lacZ-reporter studies, and demonstrate that Ni(2+) is directly involved in the derepression of the AdcR regulon via the Zn(2+)-dependent repressor AdcR, and has an opposite effect on the expression of the AdcR regulon compared to Zn(2+).
通过转录组学方法，我们通过在高细胞外浓度的Ni(2+)存在下鉴定几个差异表达的基因/操纵子，阐明了Ni(2+)对肺炎链球菌D39全局基因表达的影响。属于AdcR调控子（adcRCBA、adcAII-phtD、phtA、phtB和phtE）和PsaR调控子（pcpA、prtA和psaBCA）的基因在Ni(2+)存在下高度上调。我们通过使用电感耦合等离子体质谱分析、电泳迁移率变动分析和转录lacZ报告基因研究，进一步研究了Ni(2+)在AdcR调控子调节中的作用，并证明Ni(2+)通过锌离子依赖的阻遏物AdcR直接参与AdcR调控子的去阻遏，并且与锌离子相比，对AdcR调控子的表达具有相反的作用。
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