Exploring Fur regulon in Escherichia coli
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ABSTRACT:
ORGANISM(S): Escherichia coli
PROVIDER: GSE175957 | GEO | 2023/06/01
REPOSITORIES: GEO
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Project description:Exploring Fur regulon in Escherichia coli
| PRJNA734352 | ENA
Project description:While global transcription factors (TFs) have been studied extensively in Escherichia coli model strains, conservation and diversity in TF regulation between strains is still unknown. Here we use a combination of ChIP-exo--to define ferric uptake regulator (Fur) binding sites--and differential gene expression--to define the Fur regulon in nine E. coli strains. We then define a pan-regulon consisting of 469 target genes that includes all Fur target genes in all nine strains. The pan-regulon is then divided into the core regulon (target genes found in all the strains, n=36), the accessory regulon (target found in two to eight strains, n=158) and the unique regulon (target genes found in one strain, n=275). Thus, there is a small set of Fur regulated genes common to all nine strains, but a large number of regulatory targets unique to a particular strain. Many of the unique regulatory targets are genes unique to that strain. This first-established pan-regulon reveals a common core of conserved regulatory targets and significant diversity in transcriptional regulation amongst E. coli strains, reflecting diverse niche specification and strain history.
2023-08-04 | GSE223483 | 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:Wildtype G27 and it's Fur mutant derivative were exposed to pH 5.0 for the indicated length of time. Bacterial cells in the exponential phase of growth (denoted log) and stationary phase of growth were used. fur1 denotes a single fur mutant while fur2 denotes an additional fur mutant. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs
2006-02-03 | GSE4160 | 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:In Neisseria gonorrhoeae, Fur (ferric uptake regulator) protein regulates iron homeostasis gene expression through binding to conserved sequences in promoters of iron-responsive genes. We have expanded the gonococcal Fur regulon using a custom microarray to monitor iron-responsive gene expression throughout the growth curve combined with a genome-wide in silico analysis to predict Fur boxes (FB), and in vivo FuRTA assays to detect genes able to bind Fur. Keywords: time course: (1hr ,2hr, 3hr, 4hr)
2010-01-01 | GSE16352 | GEO
Project description:Wildtype G27 and it's Fur mutant derivative were exposed to pH 5.0 for the indicated length of time. Bacterial cells in the exponential phase of growth (denoted log) and stationary phase of growth were used. fur1 denotes a single fur mutant while fur2 denotes an additional fur mutant. An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Computed
2006-02-02 | E-GEOD-4160 | 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:Bacterial cells often modulate their transcriptional profiles in response to the changes in iron availability. Ferric uptake regulator (Fur), as a global iron biosensor, plays a central role in maintaining iron homeostasis in Bacillus subtilis. Here we utilized a high affinity Fe2+ efflux transporter, Listeria monocytogenes FrvA, as an inducible genetic tool to deplete intracellular iron. We then characterized the responses of the Fur, FsrA, and PerR regulons as cells transition from iron sufficiency to deficiency. Our results indicate that the Fur regulon is derepressed in three distinct waves. First, elemental iron uptake (ywbLMN), ferric citrate uptake (ymfCDEF-yhfQ), and petrobactin uptake (yclNOPQ) systems are induced to prevent iron deficiency. Second, B. subtilis synthesizes its own siderophore bacillibactin (dhbACEBF) and turns on bacillibactin uptake (feuABC-yusV) along with flavodoxin (ykuNOP) and hydroxamate siderophore uptake (fhuBCGD-yxeB) to scavenge iron from the environment. Third, as iron levels decline further, an iron sparing response (fsrA, fbpAB, and fbpC) is induced to block the translation of nonessential iron-using proteins and permit only essential iron-dependent enzymes to utilize the limited iron. ChIP experiments demonstrate that in vivo occupancy of Fur correlates with derepression of each operon, and the graded response observed here results, at least in part, from higher affinity binding of Fur to the late induced genes. These results provide insights into the distinct roles of Fur-regulated target genes as intracellular iron levels decline.
2017-06-30 | GSE100668 | 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