ArticleFrontiers in cellular and infection microbiology2015
The Regulation of the AdcR Regulon in Streptococcus pneumoniae Depends Both on Zn(2+)- and Ni(2+)-Availability.
Article in Frontiers in cellular and infection microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 64 citations in OpenAlex.
- AdcBC-dependent zinc uptake influences physiological responses inJournal of oral microbiology · 2026Article
- Identification ofJournal of proteome research · 2025Article
- Adaptation to zinc restriction inmSphere · 2024Article
- Calorimetric analysis of AdcR and its interactions with zinc(II) and DNA.Journal of inorganic biochemistry · 2023Article
- TheMicrobiology spectrum · 2023Article
- Pneumococcal Surface Proteins as Virulence Factors, Immunogens, and Conserved Vaccine Targets.Frontiers in cellular and infection microbiology · 2022Review
- Article
- Dietary zinc and the control of Streptococcus pneumoniae infection.PLoS pathogens · 2019Article
- PmtA functions as a ferrous iron and cobalt efflux pump inEmerging microbes & infections · 2019Article
- Zinc-Dependent Transcriptional Regulation inFrontiers in microbiology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
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+).
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