Escherichia coli str. K-12 substr. MG1655
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PROVIDER: PRJNA301960 | ENA |
REPOSITORIES: ENA
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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
Project description:As descirbed in the manuscript "The impact of anaerobiosis on expression of the iron-responsive Fur and RyhB Regulons" we profiled the gene expression of E. coli K12 during aerobic or anaerobic growth and in the presence or absence of the transcription factor Fur and/or the small RNA RyhB.
2015-12-01 | GSE74930 | GEO
Project description:The impact of anaerobiosis on expression of the iron-responsive Fur and RyhB Regulons [ChIP-chip]
| PRJNA301962 | ENA
Project description:The impact of anaerobiosis on expression of the iron-responsive Fur and RyhB Regulons [ChIP-seq]
| PRJNA301961 | ENA
Project description:The impact of anaerobiosis on expression of the iron-responsive Fur and RyhB Regulons
| PRJNA301932 | ENA
Project description:Here we dissected a regulatory network directed by the conserved iron homeostasis regulator, Ferric Uptake Regulator (Fur), in uropathogenic E. coli strain CFT073. Comparing anaerobic genome-scale Fur DNA binding, with Fur dependent transcript expression and protein levels of the uropathogen to that of commensal E. coli K-12 strain MG1655, showed that the Fur regulon of the core genome is conserved but also includes genes within the pathogenicity/genetic islands. Unexpectedly, regulons indicative of amino acid limitation and the general stress response were also indirectly activated in the uropathogen fur mutant, suggesting that induction of the Fur regulon increases amino acid demand. Using RpoS levels as a proxy, addition of amino acids mitigated the stress. In addition, iron chelation increased RpoS to the same levels as in the fur mutant. The increased amino acid demand of the fur mutant or iron chelated cells was exacerbated by aerobic conditions, which could be partly explained by the O 2 -dependent synthesis of the siderophore aerobactin, encoded within a pathogenicity island. Taken together, this data suggest in the iron-poor environment of the urinary tract, amino acid availability could play a role in the proliferation of this uropathogen, particularly if there is sufficient O 2 to produce aerobactin.
2020-05-27 | PXD017582 | Pride
Project description:RyhB is a non-coding RNA regulated by the Fur repressor. It has previously been shown to cause the rapid degradation of a number of mRNAs that encode proteins that utilize iron. Here we examine the effect of ectopic RyhB production on global gene expression by microarray analysis. Many of the previously identified targets were found, as well as other mRNAs encoding iron-binding proteins, bringing the total number of regulated operons to at least 18, encoding 56 genes. The two major operons involved in Fe-S cluster assembly showed different behavior; the isc operon appears to be a direct target of RyhB action, while the suf operon does not. This is consistent with previous findings suggesting that the suf genes but not the isc genes are important for Fe-S cluster synthesis under iron-limiting conditions, presumably for essential iron-binding proteins. In addition, we observed repression of Fur-regulated genes upon RyhB expression, interpreted as due to intracellular iron-sparing resulting from reduced synthesis of iron-binding proteins. Our results demonstrate the broad effects of a single non-coding RNA on iron homeostasis. Keywords: RNA degradation, iron stavation, RyhB small RNA, iron-using proteins
2005-08-31 | GSE3105 | GEO
Project description:RyhB is a non-coding RNA regulated by the Fur repressor. It has previously been shown to cause the rapid degradation of a number of mRNAs that encode proteins that utilize iron. Here we examine the effect of ectopic RyhB production on global gene expression by microarray analysis. Many of the previously identified targets were found, as well as other mRNAs encoding iron-binding proteins, bringing the total number of regulated operons to at least 18, encoding 56 genes. The two major operons involved in Fe-S cluster assembly showed different behavior; the isc operon appears to be a direct target of RyhB action, while the suf operon does not. This is consistent with previous findings suggesting that the suf genes but not the isc genes are important for Fe-S cluster synthesis under iron-limiting conditions, presumably for essential iron-binding proteins. In addition, we observed repression of Fur-regulated genes upon RyhB expression, interpreted as due to intracellular iron-sparing resulting from reduced synthesis of iron-binding proteins. Our results demonstrate the broad effects of a single non-coding RNA on iron homeostasis. Experiment Overall Design: Derivatives of MG1655 carrying either pBAD-ryhB or the control vector pNM12 were used in all experiments. Experiment Overall Design: The strains used contain the (delta)ara714 allele to prevent catabolism of arabinose and the (delta)ryhB::cat allele to restrict RyhB expression to the inducible pBAD-ryhB vector. Experiment Overall Design: Overnight bacterial cultures were incubated in LB media with ampicillin at a final concentration of 50 ug/mL at 37oC and diluted 1000-fold into 50 mL of fresh LB-ampicillin media at 37oC with agitation. To induce RyhB expression, cultures carrying the pBAD-ryhB construct were grown to an O.D.600 of 0.5 and arabinose was added to the culture at a final concentration of 0.1%. In some experiments, 50 uM FeSO4 was added to the new culture after dilution from overnight culture. Total RNA was extracted from cells at the indicated time using the hot phenol procedure.
2007-09-21 | E-GEOD-3105 | biostudies-arrayexpress
Project description:Porphyromonas gingivalis is a major pathogen associated with the microbial biofilm-mediated disease chronic periodontitis. P. gingivalis has an obligate requirement for iron and protoporphyrin IX which it satisfies by transporting heme and iron liberated from the human host. The level of cellular iron in P. gingivalis affects the expression of a distinct iron-associated regulon of 64 genes and low iron invokes an iron sparing response. Iron homeostasis is usually mediated in Gram-negative bacteria at the transcriptional level by the Ferric Uptake Regulator (Fur). There is a single predicted P. gingivalis Fur superfamily orthologue named Har (heme associated regulator) that lacks the conserved metal binding residues found in other Fur orthologues. We show that Har binds both heme and ferrous iron resulting in a conformational change in the protein. Har was unable to complement the Escherichia coli H1780 fur mutant and there was no change in cellular metal content in a P. gingivalis Har mutant compared with the wild-type. The Har regulon of 44 genes is not predicted to play a role in iron homeostasis. Together these data indicated that Har does not regulate iron homeostasis in P. gingivalis. However, Har was required for heme-responsive biofilm development and its regulon overlapped P. gingivalis regulons previously identified after growth in heme limitation or as a homotypic biofilm. P. gingivalis is unique as an iron-dependent Gram-negative bacterium with a single heme-binding Fur superfamily orthologue, Har, that does not regulate iron homeostasis.
2015-04-01 | GSE37099 | GEO