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Transcriptome analysis of NTHi 86-028NPrpsL, NTHi 86-028NPrpsL∆fur, NTHi 86-028NPrpsL∆fur∆hrrF, NTHi 86-028NPrpsL∆fur∆hrrF3' strains

ABSTRACT: Nontypeable Haemophilus influenzae (NTHi) is a commensal microorganism of the normal human nasopharyngeal flora, yet also an opportunistic pathogen of the upper and lower respiratory tracts. Changes in gene expression patterns in response to host microenvironments are likely critical for survival. One such system of gene regulation is the ability to carefully regulate iron uptake. A central regulatory system that controls iron uptake, mediated by the ferric uptake regulator Fur, is present in multiple bacteria, including NTHi. Previous work has identified a small RNA, HrrF, that is Fur-regulated in NTHi 86-028NPrpsL.To understand the contribution made by HrrF to gene regulation in NTHi, hrrF was deleted in the NTHi strain 86-028NPrpsL∆fur. Using RNA-Seq, we identified protein-encoding genes whose expression was repressed or activated by HrrF.

ORGANISM(S): Haemophilus influenzae

PROVIDER: GSE58891 | GEO | 2014/08/26

SECONDARY ACCESSION(S): PRJNA253820

REPOSITORIES: GEO

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Transcriptome analysis of NTHi 86-028NPrpsL, NTHi 86-028NPrpsLM-bM-^HM-^Ffur, NTHi 86-028NPrpsLM-bM-^HM-^FfurM-bM-^HM-^FhrrF, NTHi 86-028NPrpsLM-bM-^HM-^FfurM-bM-^HM-^FhrrF3' strains

Project description:Nontypeable Haemophilus influenzae (NTHi) is a commensal microorganism of the normal human nasopharyngeal flora, yet also an opportunistic pathogen of the upper and lower respiratory tracts. Changes in gene expression patterns in response to host microenvironments are likely critical for survival. One such system of gene regulation is the ability to carefully regulate iron uptake. A central regulatory system that controls iron uptake, mediated by the ferric uptake regulator Fur, is present in multiple bacteria, including NTHi. Previous work has identified a small RNA, HrrF, that is Fur-regulated in NTHi 86-028NPrpsL.To understand the contribution made by HrrF to gene regulation in NTHi, hrrF was deleted in the NTHi strain 86-028NPrpsLM-bM-^HM-^Ffur. Using RNA-Seq, we identified protein-encoding genes whose expression was repressed or activated by HrrF. These data comprise transcriptional anaylses of an rpsL mutant of 86-028NP, an isogenic fur mutant of 86-028NPrpsL, an isogenic fur mutant of 86-028NPrpsL also containing a full deletion of hrrF, and an isogenic fur mutant of 86-028NPrpsL also containing a deletion of only the 3' portion of hrrF. All strains were grown in defined medium containing 10 M-BM-5g/ml human hemoglobin to mid-log phase. Cells were then harvested and RNA extracted. A total of three biological replicates were generated for these analyses. Analysis of transcriptomes using the Illumina HiSeq 2000 of four strains of nontypeable Haemophilus influenzae which include NTHi 86-028NPrpsL, NTHi 86-028NPrpsLM-bM-^HM-^Ffur, NTHi 86-028NPrpsLM-bM-^HM-^FfurM-bM-^HM-^FhrrF, and NTHi 86-028NPrpsLM-bM-^HM-^FfurM-bM-^HM-^FhrrF3' strains. For each strain three biological replicates were analyzed.

2014-08-26 | E-GEOD-58891 | biostudies-arrayexpress

Haemophilus influenzae 86-028NP

Project description:Transcriptome analysis of NTHi 86-028NPrpsL, NTHi 86-028NPrpsL∆fur, and NTHi 86-028NPrpsL∆fur(pT-fur) strains Nontypeable Haemophilus influenzae (NTHi) is a commensal microorganism of the normal human nasopharyngeal flora, yet also an opportunistic pathogen of the upper and lower respiratory tracts. Changes in gene expression patterns in response to host microenvironments are likely critical for survival. One such system of gene regulation is the ability to carefully regulate iron uptake. A central regulatory system that controls iron uptake, mediated by the ferric uptake regulator Fur, is present in multiple bacteria, including NTHi. To understand the regulation of iron homeostasis in NTHi, fur was deleted in the NTHi strain 86-028NPrpsL. Using RNA-Seq, we identified both protein-encoding and small RNA genes whose expression was repressed or activated by Fur. Overall design: These data comprise transcriptional anaylses of an rpsL mutant of 86-028NP, an isogenic fur mutant of 86-028NPrpsL and a complemented fur mutant strain. All strains were grown in defined medium containing 10 µg/ml human hemoglobin to mid-log phase. Cells were then harvested and RNA extracted. A total of three biological replicates were generated for these analyses. Analysis of transcriptomes using the Illumina HiSeq 2000 of three strains of nontypeable Haemophilus influenzae which include NTHi 86-028NPrpsL, NTHi 86-028NPrpsL∆fur, and NTHi 86-028NPrpsL∆fur(pT-fur) strains. For each strain three biological replicates were analyzed

2015-07-01 | E-GEOD-58890 | biostudies-arrayexpress

Haemophilus influenzae 86-028NP

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2013-02-05 | GSE39874 | GEO

Fur regulation in nontyepable Haemophilus influenzae

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Project description:The purpose of the present study was to investigate the impact of heat stress for increasing imipenem susceptibility in imipenem resistant nontypeable Haemophilus influenzae (NTHi).

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Project description:Nontypeable Haemophilus influenzae (NTHi) is a pathobiont which chronically colonises the airway of individuals with chronic respiratory disease. It is unclear how NTHi persists in the airway, however accumulating evidence suggests that NTHi can invade and persist within macrophages. To better understand the mechanisms of NTHi persistence within macrophages, this work developed an in vitro model of NTHi intracellular persistence using human monocyte-derived macrophages (MDM). Dual RNA Sequencing was used to assess MDM and NTHi transcriptomic regulation occurring simultaneously during NTHi persistence. This work demonstrates that NTHi can invade and persist within human macrophages. Macrophages activate innate immune responses, whereas NTHi persistence was facilitated by transcriptomic adaptations in bacterial metabolic, stress response and ribosome pathways. This research provides transcriptomic insights into NTHi-macrophage interactions, enhances our understanding of how NTHi can utilise host immune cells to chronically colonise the airway and identifies potential bacterial gene pathways that may be attractive therapeutic targets

2021-08-23 | GSE180166 | GEO

Bacillus subtilis CU1065: WT vs fur, fur vs fur fsrA, fur vs fur fbpAB, fur vs fur fbpC, and fur vs fur fbpABC

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

The Graded Response of Fur Regulon to Iron Limitation in Bacillus subtilis

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

Haemophilus influenzae

Project description:Transcriptome analysis of NTHi 86-028NPrpsL, NTHi 86-028NPrpsL∆fur, NTHi 86-028NPrpsL∆fur∆hrrF, NTHi 86-028NPrpsL∆fur∆hrrF3' strains

| PRJNA253820 | ENA

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