Transcriptome Profile of C. Pseudotuberculosis in Response to Iron Limitation: Differential gene expression of Iron and DtxR regulated genes
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ABSTRACT:
ORGANISM(S): Corynebacterium pseudotuberculosis
PROVIDER: GSE114125 | GEO | 2019/07/31
REPOSITORIES: GEO
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Project description:The data set comprises results from the whole cellular proteome, secreted proteins and proteins located on the bacterial surface of Corynebacterium pseudotuberculosis. The theroretical proteome was created from genome analysis and characterized using bioinformatical analysis.
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Project description:Pupylation is a posttranslational protein modification in bacteria resembling ubiquitination in eukaryotes. The prokaryotic ubiquitin-like protein Pup is covalently attached to other proteins via an isopeptide bond between its carboxyterminal glutamate residue and a lysine residue in the target. In mycobacteria, pupylation was shown to mark proteins for unfolding by the ATPase Mpa and subsequent degradation by the proteasome. However, the occurrence of pupylation in species without a proteasome like Corynebacterium glutamicum suggests that degradation may not be the only fate of pupylated proteins. The Îpup mutant senses a stronger iron limitation than the wild type. Among the 125 genes showing at least 2-fold changes in transcript levels in the Îpup mutant (p-value ⤠0.05) were 54% of all genes known to be regulated by the master regulator of iron homeostasis DtxR (Brune et al., 2006; Wennerhold and Bott, 2006). Except for ftn, which is activated by DtxR and showed a 2-fold decreased mRNA level, the other DtxR target genes showed increased mRNA levels in the Îpup strain. These included ripA, encoding a transcriptional regulator of iron proteins, which represses a number of prominent iron-containing proteins under iron limitation, such as aconitase or succinate dehydrogenase (Wennerhold et al., 2005). 79% of the known RipA target genes showed decreased mRNA levels in the Îpup strain. DNA microarray analyses were performed to compare the mRNA levels of the C. glutamicum Îpup mutant and its parent wild type under iron-limited conditions. The two strains precultivated in CGXII medium with 4% (w/v) glucose and 1 µM FeSO4 were inoculated into fresh medium to an OD600 of 1, cultured for 2 h, and harvested on ice by centrifugation (5 min at 4,000 g and 4°C). Please note that the GPL16989 array design comprises oligos for 4 different bacterial genomes. In the GPR-files in this study, all IDs/Names (oligonucleotides) which are not from the host C. glutamicum were replaced by the text EMPTY since only C. glutamicum expression was analyzed.
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Project description:Pupylation is a posttranslational protein modification in bacteria resembling ubiquitination in eukaryotes. The prokaryotic ubiquitin-like protein Pup is covalently attached to other proteins via an isopeptide bond between its carboxyterminal glutamate residue and a lysine residue in the target. In mycobacteria, pupylation was shown to mark proteins for unfolding by the ATPase Mpa and subsequent degradation by the proteasome. However, the occurrence of pupylation in species without a proteasome like Corynebacterium glutamicum suggests that degradation may not be the only fate of pupylated proteins. The Δpup mutant senses a stronger iron limitation than the wild type. Among the 125 genes showing at least 2-fold changes in transcript levels in the Δpup mutant (p-value ≤ 0.05) were 54% of all genes known to be regulated by the master regulator of iron homeostasis DtxR (Brune et al., 2006; Wennerhold and Bott, 2006). Except for ftn, which is activated by DtxR and showed a 2-fold decreased mRNA level, the other DtxR target genes showed increased mRNA levels in the Δpup strain. These included ripA, encoding a transcriptional regulator of iron proteins, which represses a number of prominent iron-containing proteins under iron limitation, such as aconitase or succinate dehydrogenase (Wennerhold et al., 2005). 79% of the known RipA target genes showed decreased mRNA levels in the Δpup strain.
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Project description:HupB is a 28 kDa in Mycobacterium tuberculosis that is co-expressed with the siderophores mycobactin and carboxymycobactin upon iron limitation. High levels of all the three components are seen in low iron (LI; 0.02 µg Fe / mL) organisms, with negligible expression in high iron organisms (HI; 8 µg Fe / mL). We generated a hupB knock out mutant of M. tuberculosis (H37Rv ∆ hupB) and studied the differential expression of genes upon iron limitation in the WT H37Rv and the mutant. The RNA transcripts of the WT H37Rv, grown under high and low iron conditions of growth were isolated and subjected to microarray analysis to identify the iron-regulated genes and second, the differential expression of genes in iron-limited H37Rv ∆ hupB vs iron-limited WT H37Rv was analysed. Microarray analysis was done commercially by Genotypic Technology (Bangalore, India), an authorised service provider for Agilent Technologies. The study revealed the up-regulation of all the mbt genes of the mycobactin biosynthetic machinery in LI - H37Rv and several other reported iron-regulated genes. The salient feature of this study is the failure of LI - H37Rv ∆ hupB to show any up-regulation of the mbt genes as compared to LI - H37Rv. Among several other genes influenced by HupB, the mutant strain showed low levels of mmpL5 and mmpS5 transcripts, whose expressed products are reported to be associated with siderophore transport and biosynthesis.
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Project description:The Twin-arginine translocation (Tat) system promotes secretion of folded proteins that in bacteria are identified via an N-terminal signal peptide. Tat systems are associated with virulence in many bacterial pathogens and our previous studies revealed that Tat deficient Yersinia pseudotuberculosis was severely attenuated for virulence. However, in silico predictions did not reveal any obvious virulence factors among the potential Tat substrates encoded by Y. pseudotuberculosis. Aiming to identify Tat dependent pathways and phenotypes of relevance for in vivo infection, we analysed the global transcriptome of parental and ∆tatC mutant strains of Y. pseudotuberculosis during exponential and stationary growth at 26°C and 37°C. The most significant changes in the transcriptome of the ∆tatC mutant were seen at 26°C during stationary phase growth and these included the altered expression of genes related to virulence, stress responses and metabolism. Subsequent phenotypic analysis based on these transcriptome changes revealed several novel Tat dependent phenotypes including decreased YadA expression, impaired growth under iron-limiting and high copper concentrations as well as sensitivity to acidic pH and SDS. Several functionally related Tat substrates were also verified to contribute to these phenotypes. Interestingly, the phenotypes of the Tat deficient strain were generally more pronounced than for the individual mutants of the genes encoding the specific Tat substrates. Altogether, this provides new insight into the impact of Tat deficiency on in vivo fitness and survival/replication of Y. pseudotuberculosis during infection.
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Project description:The Twin-arginine translocation (Tat) system promotes secretion of folded proteins that in bacteria are identified via an N-terminal signal peptide. Tat systems are associated with virulence in many bacterial pathogens and our previous studies revealed that Tat deficient Yersinia pseudotuberculosis was severely attenuated for virulence. However, in silico predictions did not reveal any obvious virulence factors among the potential Tat substrates encoded by Y. pseudotuberculosis. Aiming to identify Tat dependent pathways and phenotypes of relevance for in vivo infection, we analysed the global transcriptome of parental and ∆tatC mutant strains of Y. pseudotuberculosis during exponential and stationary growth at 26°C and 37°C. The most significant changes in the transcriptome of the ∆tatC mutant were seen at 26°C during stationary phase growth and these included the altered expression of genes related to virulence, stress responses and metabolism. Subsequent phenotypic analysis based on these transcriptome changes revealed several novel Tat dependent phenotypes including decreased YadA expression, impaired growth under iron-limiting and high copper concentrations as well as sensitivity to acidic pH and SDS. Several functionally related Tat substrates were also verified to contribute to these phenotypes. Interestingly, the phenotypes of the Tat deficient strain were generally more pronounced than for the individual mutants of the genes encoding the specific Tat substrates. Altogether, this provides new insight into the impact of Tat deficiency on in vivo fitness and survival/replication of Y. pseudotuberculosis during infection.
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Project description:The Twin-arginine translocation (Tat) system promotes secretion of folded proteins that in bacteria are identified via an N-terminal signal peptide. Tat systems are associated with virulence in many bacterial pathogens and our previous studies revealed that Tat deficient Yersinia pseudotuberculosis was severely attenuated for virulence. However, in silico predictions did not reveal any obvious virulence factors among the potential Tat substrates encoded by Y. pseudotuberculosis. Aiming to identify Tat dependent pathways and phenotypes of relevance for in vivo infection, we analysed the global transcriptome of parental and ∆tatC mutant strains of Y. pseudotuberculosis during exponential and stationary growth at 26°C and 37°C. The most significant changes in the transcriptome of the ∆tatC mutant were seen at 26°C during stationary phase growth and these included the altered expression of genes related to virulence, stress responses and metabolism. Subsequent phenotypic analysis based on these transcriptome changes revealed several novel Tat dependent phenotypes including decreased YadA expression, impaired growth under iron-limiting and high copper concentrations as well as sensitivity to acidic pH and SDS. Several functionally related Tat substrates were also verified to contribute to these phenotypes. Interestingly, the phenotypes of the Tat deficient strain were generally more pronounced than for the individual mutants of the genes encoding the specific Tat substrates. Altogether, this provides new insight into the impact of Tat deficiency on in vivo fitness and survival/replication of Y. pseudotuberculosis during infection.
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