Transcriptional analysis of the Neisseria gonorrhoeae Fur regulon
Ontology highlight
ABSTRACT:
ORGANISM(S): Neisseria gonorrhoeae Neisseria meningitidis Neisseria gonorrhoeae FA 1090
PROVIDER: GSE16352 | GEO | 2010/01/01
SECONDARY ACCESSION(S): PRJNA115309
REPOSITORIES: GEO
Similar Datasets
Project description:In this study wild-type, fur mutant, and complemented fur mutant strains of the human pathogen Neisseria gonorrhoeae F62 were grown under high (100 uM iron) or low (100 uM desferal) iron conditions to identify genes whose expression was regulated by iron and/or Fur
2016-06-09 | GSE83138 | GEO
Project description:In this study wild-type, fur mutant, and complemented fur mutant strains of the human pathogen Neisseria gonorrhoeae F62 were grown under high (100 uM iron) or low (100 uM desferal) iron conditions to identify genes whose expression was regulated by iron and/or Fur. This study looked at the response 3 hours after the addition of iron or desferal.
2020-01-13 | GSE143480 | GEO
Project description:Previous studies have shown that the MpeR transcriptional regulator produced by Neisseria gonorrhoeae represses expression of mtrF, which encodes a putative inner membrane protein that works with the MtrC-MtrD-MtrE efflux pump to allow gonococci to resist high levels of multiple hydrophobic antimicrobials. Regulation of mpeR has been reported to occur by an iron-dependent mechanism involving Fur (Ferric uptake regulator). Collectively, these observations suggest the presence of an interconnected regulatory system in gonococci that modulates expression of drug efflux pump protein-encoding genes in an iron-responsive manner. Herein, we describe this connection and report that levels of gonococcal resistance to a substrate of the mtrCDE-encoded efflux pump can be modulated by MpeR and the availability of free iron. Using microarray analysis, we found that the mtrR gene, which encodes the direct transcriptional repressor (MtrR) of mtrCDE, is an MpeR-repressed determinant in the late-logarithmic phase of growth when free iron levels would be reduced due to bacterial consumption. MpeR-mediated repression of mtrR appeared to be direct, as judged by DNA-binding analyses, and was enhanced by conditions of iron-limitation, which resulted in increased expression of the mtrCDE efflux pump operon. Taken together, our results indicate that both genetic and physiologic parameters can influence expression of the mtr efflux system and that these can modulate levels of gonococcal susceptibility to efflux pump substrates. two strains, two growth phases, three replicates each.
2012-04-03 | E-GEOD-32717 | biostudies-arrayexpress
Project description:Previous studies have shown that the MpeR transcriptional regulator produced by Neisseria gonorrhoeae represses expression of mtrF, which encodes a putative inner membrane protein that works with the MtrC-MtrD-MtrE efflux pump to allow gonococci to resist high levels of multiple hydrophobic antimicrobials. Regulation of mpeR has been reported to occur by an iron-dependent mechanism involving Fur (Ferric uptake regulator). Collectively, these observations suggest the presence of an interconnected regulatory system in gonococci that modulates expression of drug efflux pump protein-encoding genes in an iron-responsive manner. Herein, we describe this connection and report that levels of gonococcal resistance to a substrate of the mtrCDE-encoded efflux pump can be modulated by MpeR and the availability of free iron. Using microarray analysis, we found that the mtrR gene, which encodes the direct transcriptional repressor (MtrR) of mtrCDE, is an MpeR-repressed determinant in the late-logarithmic phase of growth when free iron levels would be reduced due to bacterial consumption. MpeR-mediated repression of mtrR appeared to be direct, as judged by DNA-binding analyses, and was enhanced by conditions of iron-limitation, which resulted in increased expression of the mtrCDE efflux pump operon. Taken together, our results indicate that both genetic and physiologic parameters can influence expression of the mtr efflux system and that these can modulate levels of gonococcal susceptibility to efflux pump substrates.
2012-04-04 | GSE32717 | GEO
Project description:Global tranascriptional profiling of Bacillus subtilis cells comparing fur mutant to mutants of the iron-sparing response: fur fsrA double mutant, fur fbpAB triple mutant, fur fbpC double mutant, and fur fbpABC quadruple mutant Abstract of associated manuscript: The Bacillus subtilis ferric uptake regulator (Fur) protein is the major sensor of cellular iron status. When iron is limiting for growth, derepression of the Fur regulon increases the cellular capacity for iron uptake and mobilizes an iron-sparing response mediated, in large part, by a small non-coding RNA named FsrA. FsrA functions together with three small, basic proteins (FbpABC) to repress many "low-priority" iron-containing enzymes. We have used transcriptome analyses to define the scope of the iron-sparing response and to define subsets of genes dependent on either FbpAB or FbpC for their repression. Enzymes of the tricarboxylic acid cycle, including both aconitase and succinate dehydrogenase, are major targets of FsrA-mediated repression and, as a consequence, flux through this pathway is significantly decreased under iron limitation. FsrA also mediates a physiologically significant repression of iron-sulfur containing enzymes required for ammonium assimilation (the GltAB glutamate synthase) and catabolism of lactic acid (LutABC). Repression of the lutABC operon requires both FsrA and FbpB which supports a model in which the Fbp proteins function to enable repression of subsets of the FsrA regulon.
2011-02-19 | GSE27416 | GEO
Project description:In the alpha subclass of proteobacteria iron homeostasis is controlled by diverse iron responsive regulators. Caulobacter crescentus, an important freshwater α-proteobacterium, uses the ferric uptake repressor (Fur) for such purpose. However, the impact of the iron availability on the C. crescentus transcriptome and an overall perspective of the regulatory networks involved remain unknown. In this work we report the identification of iron-responsive and Fur-regulated genes in C. crescentus using microarray-based global transcriptional analyses. We identify 46 genes that were strongly upregulated both by mutation of fur and by iron limitation condition. Among them, there are genes involved in iron uptake (four TonB dependent receptor gene clusters, feoAB), riboflavin biosynthesis and some genes encoding hypothetical proteins. Most of these genes are associated with Fur binding sites, implicating them as direct targets of Fur-mediated repression. These data were validated by β-galactosidase and EMSA assays for two operons encoding putative transporters. The role of Fur as a positive regulator is also evident, given that 50 genes were downregulated both by mutation of fur and under low-iron condition. As expected, this group includes many genes involved in energy metabolism, mostly iron-using enzymes. Surprisingly, are also included in this group many genes encoding TonB dependent receptors and the genes fixK, fixT and ftrB encoding an oxygen signaling network required for growth during hypoxia. Bioinformatics analyses performed in the promoters of these genes suggest that positive regulation by Fur is mainly indirect. In addition to the Fur modulon, iron limitation altered expression of more 103 genes, including upregulation of genes involved in Fe-S cluster assembly, oxidative stress and heat shock response, as well as downregulation of genes implicated in amino acid metabolism, chemotaxis and motility. Altogether, our results showed that adaptation of C. crescentus to iron limitation involves increasing the transcription of iron-acquisition systems and decreasing the production of iron-using proteins as a general strategy
2013-08-15 | GSE45653 | GEO
Project description:In the alpha subclass of proteobacteria iron homeostasis is controlled by diverse iron responsive regulators. Caulobacter crescentus, an important freshwater α-proteobacterium, uses the ferric uptake repressor (Fur) for such purpose. However, the impact of the iron availability on the C. crescentus transcriptome and an overall perspective of the regulatory networks involved remain unknown. In this work we report the identification of iron-responsive and Fur-regulated genes in C. crescentus using microarray-based global transcriptional analyses. We identify 46 genes that were strongly upregulated both by mutation of fur and by iron limitation condition. Among them, there are genes involved in iron uptake (four TonB dependent receptor gene clusters, feoAB), riboflavin biosynthesis and some genes encoding hypothetical proteins. Most of these genes are associated with Fur binding sites, implicating them as direct targets of Fur-mediated repression. These data were validated by β-galactosidase and EMSA assays for two operons encoding putative transporters. The role of Fur as a positive regulator is also evident, given that 50 genes were downregulated both by mutation of fur and under low-iron condition. As expected, this group includes many genes involved in energy metabolism, mostly iron-using enzymes. Surprisingly, are also included in this group many genes encoding TonB dependent receptors and the genes fixK, fixT and ftrB encoding an oxygen signaling network required for growth during hypoxia. Bioinformatics analyses performed in the promoters of these genes suggest that positive regulation by Fur is mainly indirect. In addition to the Fur modulon, iron limitation altered expression of more 103 genes, including upregulation of genes involved in Fe-S cluster assembly, oxidative stress and heat shock response, as well as downregulation of genes implicated in amino acid metabolism, chemotaxis and motility. Altogether, our results showed that adaptation of C. crescentus to iron limitation involves increasing the transcription of iron-acquisition systems and decreasing the production of iron-using proteins as a general strategy Two experimental procedures, each of them performed in two replicates. A total of four independent biological samples were used
2013-08-15 | E-GEOD-45653 | biostudies-arrayexpress
Project description:Global transcriptional profiling of Bacillus subtilis cells comparing fur mutant to mutants of the iron-sparing response: fur fsrA double mutant, fur fbpAB triple mutant, fur fbpC double mutant, and fur fbpABC quadruple mutant fur vs fur fsrA (fsrA), fur vs fur fbpAB (AB), fur vs fur fbpC (C), and fur vs fur fbpABC (ABC). Each experiemnt (fur vs mutant) was conducted three times using three independent total RNA preparations (2 independent experiement + 1 independent dye swap).
2011-02-19 | E-GEOD-27416 | biostudies-arrayexpress
Project description:As descirbed in the manuscript "The impact of anaerobiosis on expression of the iron-responsive Fur and RyhB Regulons" we mapped the locations of Fur DNA binding in E. coli K12 under aerobic or anaerobic growth conditions and anerobic iron deficient growth conditions.
2015-12-01 | GSE74932 | GEO
Project description:As descirbed in the manuscript The impact of anaerobiosis on expression of the iron-responsive Fur and RyhB Regulons we performed a control ChIP-chip experiment in an E. coli strain lacking the transcription factor Fur to identify regions Fur-independent enrichment.
2015-12-01 | GSE74931 | GEO