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Ni2+-dependent and PsaR-mediated regulation of the virulence genes pcpA, psaBCA, and prtA in Streptococcus pneumoniae

ABSTRACT: Previous studies have shown that the transcriptional regulator PsaR regulates the expression of the PsaR regulon consisting of genes encoding choline binding protein (PcpA), the extracellular serine protease (PrtA), and the Mn2+-uptake system (PsaBCA), in the presence of manganese (Mn2+), zinc (Zn2+), and cobalt (Co2+). In this study, we explore the Ni2+-dependent regulation of the PsaR regulon. We have demonstrated by qRT-PCR analysis, metal accumulation assays, β-galactosidase assays, and electrophoretic mobility shift assays that an elevated concentration of Ni2+ leads to strong induction of the PsaR regulon. Our ICP-MS data show that the Ni2+-dependent expression of the PsaR regulon is directly linked to high, cell-associated, concentration of Ni2+, which reduces the cell-associated concentration of Mn2+. In vitro studies with the purified PsaR protein showed that Ni2+ diminishes the Mn2+-dependent interaction of PsaR to the promoter regions of its target genes, confirming an opposite effect of Mn2+ and Ni2+ in the regulation of the PsaR regulon. Additionally, the Ni2+-dependent role of PsaR in the regulation of the PsaR regulon was studied by transcriptome analysis.

ORGANISM(S): Streptococcus pneumoniae D39

PROVIDER: GSE73818 | GEO | 2015/11/20

SECONDARY ACCESSION(S): PRJNA298037

REPOSITORIES: GEO

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Ni2+-dependent and PsaR-mediated regulation of the virulence genes pcpA, psaBCA, and prtA in Streptococcus pneumoniae

Project description:Previous studies have shown that the transcriptional regulator PsaR regulates the expression of the PsaR regulon consisting of genes encoding choline binding protein (PcpA), the extracellular serine protease (PrtA), and the Mn2+-uptake system (PsaBCA), in the presence of manganese (Mn2+), zinc (Zn2+), and cobalt (Co2+). In this study, we explore the Ni2+-dependent regulation of the PsaR regulon. We have demonstrated by qRT-PCR analysis, metal accumulation assays, Î²-galactosidase assays, and electrophoretic mobility shift assays that an elevated concentration of Ni2+ leads to strong induction of the PsaR regulon. Our ICP-MS data show that the Ni2+-dependent expression of the PsaR regulon is directly linked to high, cell-associated, concentration of Ni2+, which reduces the cell-associated concentration of Mn2+. In vitro studies with the purified PsaR protein showed that Ni2+ diminishes the Mn2+-dependent interaction of PsaR to the promoter regions of its target genes, confirming an opposite effect of Mn2+ and Ni2+ in the regulation of the PsaR regulon. Additionally, the Ni2+-dependent role of PsaR in the regulation of the PsaR regulon was studied by transcriptome analysis. Comparison of the Streptococcus pneumoniae D39 wild-type vs D39 ÎpsaR in CDM Plus 0.3 mM Ni2+ Two condition design including a dye swap

2015-11-20 | E-GEOD-73818 | biostudies-arrayexpress

The regulation of the AdcR regulon in Streptococcus pneumoniae depends both on Zn2+- and Ni2+- availability

Project description:By using the transcriptomic approach, we have elucidated the effect of Ni2+ 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 Ni2+. 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 Ni2+. We have further studied the role of Ni2+ in the regulation of the AdcR regulon by using ICP-MS analysis, electrophoretic mobility shift assays and transcriptional lacZ-reporter studies, and demonstrate that Ni2+ is directly involved in the derepression of the AdcR regulon via the Zn2+-dependent repressor AdcR, and has an opposite effect on the expression of the AdcR regulon as compared to Zn2+. This SuperSeries is composed of the SubSeries listed below.

2015-11-20 | GSE73852 | GEO

D39 wild-type vs D39 ÎadcR In CDM with 0.3 mM Ni2+

Project description:By using the transcriptomic approach, we have elucidated the effect of Ni2+ 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 Ni2+. 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 Ni2+. We have further studied the role of Ni2+ in the regulation of the AdcR regulon by using ICP-MS analysis, electrophoretic mobility shift assays and transcriptional lacZ-reporter studies, and demonstrate that Ni2+ is directly involved in the derepression of the AdcR regulon via the Zn2+-dependent repressor AdcR, and has an opposite effect on the expression of the AdcR regulon as compared to Zn2+. Comparison of the Streptococcus pneumoniae D39 wild-type vs D39 ÎadcR in CDM Plus 0.3 mM Ni2+ Two condition design comparison of Wild-type strain vs mutant strain including a dye swap

2015-11-20 | E-GEOD-73851 | biostudies-arrayexpress

High Ni2+ vs Low Ni2+

Project description:By using the transcriptomic approach, we have elucidated the effect of Ni2+ 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 Ni2+. 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 Ni2+. We have further studied the role of Ni2+ in the regulation of the AdcR regulon by using ICP-MS analysis, electrophoretic mobility shift assays and transcriptional lacZ-reporter studies, and demonstrate that Ni2+ is directly involved in the derepression of the AdcR regulon via the Zn2+-dependent repressor AdcR, and has an opposite effect on the expression of the AdcR regulon as compared to Zn2+. Comparison of the Streptococcus pneumoniae D39 wild-type in CDM Plus 0.5 mM Ni and CDM plus 0 mM Ni2+ Two condition design comparison of two conditions 0.5 mM Ni2+ Vs 0 mM Ni2+ including a dye swap

2015-11-20 | E-GEOD-73850 | biostudies-arrayexpress

Transcriptome analysis of B. subtilis cells during recovery from injury after high hydrostatic pressure treatment

Project description:Vegetative cells of B. subtilis can recover from injury caused by high hydrostatic pressure (HHP) treatment at 250 MPa. DNA microarray analysis revealed that many ribosomal genes and translation relating factors (e.g. translation initiation factors) were induced during a growth-arrested phase after the HHP treatment. Expression of cold shock-responsive genes, whose products play key roles for efficient translation, and heat shock-responsive genes, whose product mediates the correct protein folding or degrades misfolded proteins, were also induced. In contrast, the expression of hpf, whose product (Hpf) is involved in ribosome inactivation through dimerization of 70S ribosomes, was repressed. Sucrose density gradient sedimentation analysis showed that ribosomes were dissociated in a pressure-dependent manner and then reconstructed during the growth-arrested phase. These results suggested that the translational machinery can be preferentially reconstructed in the HHP-injured cells. We also found that cell growth after HHP-induced injury was apparently inhibited by Mn2+ or Zn2+ supplemented to the recovery medium. Ribosome reconstruction in HHP-injured cells was significantly delayed in the presence of Mn2+ or Zn2+. Moreover, Zn2+ but not Mn2+ stimulated dimer formation of ribosomes in HHP-injured cells. This Zn2+-dependent accumulation of ribosome dimer was no longer observed in a Δhpf mutant lacking the functional Hpf. Furthermore, the growth recovery of the Δhpf mutant in the Zn2+-supplemented medium was faster than that of the parent strain. Thus, our results indicate that Zn2+ can prevent ribosome reconstruction by stimulating the Hpf-dependent ribosome dimerization, thereby inhibiting the growth recovery of the HHP-injured B. subtilis cells.

2019-10-26 | GSE126203 | GEO

The regulation of the AdcR regulon in Streptococcus pneumoniae depends both on Zn2+- and Ni2+- availability

Project description:The regulation of the AdcR regulon in Streptococcus pneumoniae depends both on Zn2+- and Ni2+- availability

| PRJNA298223 | ENA

Spneu D39 wildtype grown in GM17 versus GM17 + 0.25 mM ZnSO4

Project description:This study addresses the response of Streptococcus pneumoniae to zinc. The wild-type strain D39 was grown in GM17 and GM17 with 0.25 mM of ZnSO4. The transcriptome under these conditions was compared by using microarrays. Keywords: transcriptome analysis of D39 wild-type compared with its isogenic glnPA double mutant The wild-type strain D39 was grown in 4 biological replicates in GM17 and in GM17+0.25 mM ZnSO4 to an Optical Density at 600 nm of 0.3. From these cultures samples were prepared for transciptome determination with in-house printed microarrays covering the genomes of several S. pneumoniae species. The GM17 samples (CH1) and GM17+ZnSO4 samples (CH2) were labeled with Cy5 or Cy3. Samples were hybridized to glass-microarray slides. This work is part of a publication that is likely to be released in june/july 2008: 'Opposite effects of Mn2+ and Zn2+ on the PsaR-mediated expression of the virulence genes pcpA, prtA and psaBCA of Streptococcus pneumoniae" by Kloosterman et al.

2008-05-17 | E-GEOD-11438 | biostudies-arrayexpress

Transcriptional response of Streptococcus pneumoniae to Zn2+-limitation and the repressor/activator function of AdcR

Project description:Zinc (Zn2+) is an important trace metal ion that has been shown to regulate the expression of several (virulence) genes in streptococci. Previously, we analyzed the genome-wide response of S. pneumoniae to Zn2+-stress. In this work, we have performed a transcriptomic analysis to identify genes that are differentially expressed under intracellular Zn2+-limitation. This revealed a number of genes that are highly upregulated in the absence of extracellular Zn2+, amongst which the genes belonging to the regulon of the Zn2+-responsive repressor AdcR, like adcBCA, encoding a Zn2+-dependent ABC-uptake system, adcAII, encoding a Zn2+-binding lipoprotein, and also virulence genes belonging to the Pht family (phtA, phtB, phtD and phtE). Using transcriptome analysis, lacZ-reporter studies, in vitro DNA binding experiments, and in silico operator predictions, we show that AdcR directly represses the promoters of adcRCBA, adcAII-phtD, phtA, phtB and phtE in the presence of Zn2+. AdcR can also function as an activator, since in the presence of Zn2+ it directly induces expression of adh that encodes a Zn2+-containing alcohol dehydrogenase. In conclusion, the genome-wide transcriptional response of S. pneumoniae to Zn2+-limitation was established, which is mainly mediated via direct regulation by the Zn2+-dependent regulator AdcR. This SuperSeries is composed of the SubSeries listed below.

2011-05-13 | GSE29236 | GEO

Streptococcus pneumoniae D39

Project description:Ni2+-dependent and PsaR-mediated regulation of the virulence genes pcpA, psaBCA, and prtA in Streptococcus pneumoniae

| PRJNA298037 | ENA

Transcriptional response of Streptococcus pneumoniae to Zn2+-limitation and the repressor/activator function of AdcR

Project description:Zinc (Zn2+) is an important trace metal ion that has been shown to regulate the expression of several (virulence) genes in streptococci. Previously, we analyzed the genome-wide response of S. pneumoniae to Zn2+-stress. In this work, we have performed a transcriptomic analysis to identify genes that are differentially expressed under intracellular Zn2+-limitation. This revealed a number of genes that are highly upregulated in the absence of extracellular Zn2+, amongst which the genes belonging to the regulon of the Zn2+-responsive repressor AdcR, like adcBCA, encoding a Zn2+-dependent ABC-uptake system, adcAII, encoding a Zn2+-binding lipoprotein, and also virulence genes belonging to the Pht family (phtA, phtB, phtD and phtE). Using transcriptome analysis, lacZ-reporter studies, in vitro DNA binding experiments, and in silico operator predictions, we show that AdcR directly represses the promoters of adcRCBA, adcAII-phtD, phtA, phtB and phtE in the presence of Zn2+. AdcR can also function as an activator, since in the presence of Zn2+ it directly induces expression of adh that encodes a Zn2+-containing alcohol dehydrogenase. In conclusion, the genome-wide transcriptional response of S. pneumoniae to Zn2+-limitation was established, which is mainly mediated via direct regulation by the Zn2+-dependent regulator AdcR. Two condition design comparison of Wild-type strain including a dye swap Refer to individual Series. This SuperSeries is composed of the following subset Series: GSE29234: adcR mutant vs wild type D39 GSE29235: Low Zn vs high Zn in CDM

2011-05-13 | E-GEOD-29236 | biostudies-arrayexpress

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