The Regulation of the AdcR Regulon in Streptococcus pneumoniae Depends Both on Zn(2+)- and Ni(2+)-Availability.
Front Cell Infect Microbiol, 2015;5:91.
Manzoor I[1], Shafeeq S[2], Afzal M[1], Kuipers OP[3]
Affiliations
PMID: 26697415DOI: 10.3389/fcimb.2015.00091
Impact factor: 6.073
Abstract
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+).
Keywords: AdcR; AdcR regulon; Pht family proteins; PsaR regulon; metal homeostasis; nickel; pneumococcus; zinc
MeSH terms
Electrophoretic Mobility Shift Assay; Gene Expression Profiling; Gene Expression Regulation, Bacterial; Genes, Reporter; Mass Spectrometry; Metals, Heavy; Nickel; Regulon; Streptococcus pneumoniae; Zinc; beta-Galactosidase
More resources
Full text:
Europe PubMed Central; PubMed Central
EndNote: Download