A Novel Copper Responsive Regulon in Mycobacterium tuberculosis strains mpA and pafA
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ABSTRACT:
ORGANISM(S): Mycobacterium tuberculosis
PROVIDER: GSE24968 | GEO | 2011/11/01
SECONDARY ACCESSION(S): PRJNA131895
REPOSITORIES: GEO
Similar Datasets
Project description:In this study, we report the identification of a five-locus copper-inducible regulon in Mycobacterium tuberculosis. The identification of a copper responsive regulon unique to pathogenic Mycobacteria suggests copper homeostasis must be maintained during an infection.
2010-10-27 | GSE23498 | GEO
Project description:In this study, we report the identification of a five-locus copper-inducible regulon in Mycobacterium tuberculosis. The identification of a copper responsive regulon unique to pathogenic Mycobacteria suggests copper homeostasis must be maintained during an infection. WT and mutant Mtb cells were grown in Sauton’s minimal media to early stationary phase (OD580 = 1.5) and treated with 500 mM copper sulfate (CuSO4) for four hours or the absence.
2011-11-01 | E-GEOD-24968 | biostudies-arrayexpress
Project description:In this study, we report the identification of a five-locus copper-inducible regulon in Mycobacterium tuberculosis. The identification of a copper responsive regulon unique to pathogenic Mycobacteria suggests copper homeostasis must be maintained during an infection. WT and mutant Mtb cells were grown in Sauton's minimal media to early stationary phase (OD580 = 1.5) and treated with 500 mM copper sulfate (CuSO4) for four hours or the absence
2010-10-27 | E-GEOD-23498 | biostudies-arrayexpress
Project description:In this study, we report the identification and characterization of several regulators in Mycobacterium tuberculosis.
2010-09-29 | GSE23947 | GEO
Project description:Purpose: CsoR, a copper responsive negative regulator of Mycobacterium tuberculosis has been shown to respond to copper and bind to its own regulon in in vitro experiments. Here we examine the role of CsoR in vivo by examining the impact of deletion of csoR on the host transcriptome. Methods: csoR was knocked out of M. tuberculosis H37Rv using the specialized transduction method developed by Bardarov et al (2002), followed by removal of the hygromycin marker with plasmid pYUB870. Both wild type and confirmed csoR knockout were grown in copper free Sauton's media to late log phase before harvesting for transcriptomic studies. RNA was extracted using a modified Trizol method prior to DNAse treatment and rRNA depletion. Sequencing was done on an Illumina HiSeq 2000, filtered for quality using the FASTX-Toolkit, and mapped using Bowtie, and counts per locus generated with BedTools in the Galaxy platform. Differential expression analysis was carried out in edgeR with significantly differentially expressed genes being identified as those with ≥|2| fold differential expression between ΔcsoR and wild type strains, and an FDR < 0.05. Results: We found that 223 genes were differentially expressed between the ΔcsoR and wild type strains, 52 induced and 71 repressed. Differential expression of 10 of these genes, 6 induced and 4 repressed, was confirmed by qRT-PCR using SYBR green methodology. The only copper responsive genes identified were those within the csoR operon: csoR, Rv0968, ctpV, Rv0970, suggesting that csoR may only regulate its own operon in response to copper. Genes in the RicR regulon, another copper responsive transcriptional regulator, were not significantly differentially expressed, but some of these copper inducible genes were slightly down regulated suggesting that copper levels may be lower in the mutant strain as compared to wild type. Notably, 44 of the 48 members of the dosR regulon, responsive to hypoxic and NO stress, were induced in the mutant vs wild type suggesting that csoR is necessary for maintaining homeostasis, likely through copper regulation, within the cell. Conclusions: We have shown that CsoR is likely only directly regulating its own operon in response to copper, however it is required to maintain homeostasis, preventing a hypoxia-type stress response in the absense of copper.
2016-11-01 | GSE74323 | GEO
Project description:The host restricts Mycobacterium tuberculosis (Mtb) access of transition metal ions to inhibit its growth. Cu is essential for the survival of Mtb, but Cu excess is toxic. During co-evolution, Mtb has developed various mechanisms to maintain copper homeostasis. In this report, we firstly found Mtb Rv0102 encoded membrane protein is critical for Mycobacterium Cu uptake. The intracellular Cu level of M. smegmatis (Ms) Rv0102 homolog MSMEG_4702 knockout strain decreased threefold than the wild type, the deletion mutant was more tolerant to higher Cu level. This indicates that Rv0102 is significant for Cu homeostasis and resistance to Cu toxicity. Knocking out the homologous gene MMAR_0267 in M. marinum (Mm) also enhanced its virulence in zebrafish and improved its survival within macrophages. In THP-1 cells infected with Mm, Mm MMAR_0267 deletion mutants’ intracellular survival increased fourfolds and accompanied by less cell apoptosis. Cu deficiency down-regulates the transcription of the M. marinum virulence factor CFP-10, dampening the STING cytosolic signaling in macrophages, fewer IFN-β and less cell apoptosis. These results suggest that Cu is an important factor in inducing cell apoptosis. In summary, mycobacteria can effectively counteract the host's early key nutritional immune mechanisms by regulating copper metabolism, to increase its virulence.
2023-06-30 | GSE235754 | GEO
Project description:In this work we describe the identification of a copper-inducible regulon in Mycobacterium tuberculosis (Mtb). Among the regulated genes was Rv0190/MT0200, a paralogue of the copper metalloregulatory repressor CsoR. The five-locus regulon, which includes a gene that encodes the copper-protective metallothionein MymT, was highly induced in wild-type Mtb treated with copper, and highly expressed in an Rv0190/MT0200 mutant. Importantly, the Rv0190/MT0200 mutant was hyper-resistant to copper. The promoters of all five loci share a palindromic motif that was recognized by the gene product of Rv0190/MT0200. For this reason we named Rv0190/MT0200 RicR for regulated in copper repressor. Intriguingly, several of the RicR-regulated genes, including MymT, are unique to pathogenic Mycobacteria. The identification of a copper-responsive regulon specific to virulent mycobacterial species suggests copper homeostasis must be maintained during an infection. Alternatively, copper may provide a cue for the expression of genes unrelated to metal homeostasis, but nonetheless necessary for survival in a host.
| S-EPMC3052634 | biostudies-literature
Project description:This SuperSeries is composed of the following subset Series: GSE34919: Genome-wide Definition of the SigF Regulon in Mycobacterium tuberculosis (ChIP-chip) GSE34922: Genome-wide Definition of the SigF Regulon in Mycobacterium tuberculosis (Expression) Refer to individual Series
2012-01-20 | E-GEOD-35080 | biostudies-arrayexpress
Project description:In Saccharomyces cerevisiae, copper ions regulate gene expression through the two transcriptional activators, Ace1 and Mac1. Ace1 mediates Cu-induced gene expression in cells exposed to stressful levels of copper salts, whereas Mac1 activates a subset of genes under copper-deficient conditions. DNA microarray hybridization experiments revealed a limited set of yeast genes differentially expressed under growth conditions of excess copper or copper deficiency. Mac1 activates the expression of six S. cerevisiae genes, including CTR1, CTR3, FRE1, FRE7, YJL217w and YFR055w. Two of the last three newly identified Mac1 target genes have no known function, the third, YFR055w, is homologous to cystathionine gamma-lyase encoded by CYS3. Several genes that are differentially expressed in cells containing a constitutively active Mac1, designated Mac1up1, are not direct targets of Mac1. Induction or repression of these genes is likely a secondary effect of cells due to constitutive Mac1 activity. Elevated copper levels induced the expression of the metallothioneins CUP1 and CRS5, and two genes, FET3 and FTR1, in the iron uptake system. Cu-induced FET3 and FTR1 expression arises from an indirect Cu effect on cellular Fe pools. This study is described in more detail in Gross C et al.(2000) J Biol Chem 275:32310-6 Keywords: other
2002-02-12 | GSE26 | GEO
Project description:A novel copper-responsive regulon in Mycobacterium tuberculosis
| PRJNA130411 | ENA