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Escherichia coli str. K-12 substr. MG1655

ABSTRACT: The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli [ChIP-Seq]

PROVIDER: PRJNA200299 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR835423.fastq.gz	Fastqsanger.gz
	SRR835424.fastq.gz	Fastqsanger.gz

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Expression analysis of Escherichia coli MG1655 K-12 WT and ∆arcA mutant

Project description:Investigation of whole genome gene expression level changes in a Escherichia coli MG1655 K-12 ∆arcA mutant, compared to the wild-type strain. The mutations engineered into this strain produce a strain lacking the ArcA protein. The results are further described in the manuscript The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli

2013-10-17 | GSE46412 | GEO

ArcA Chip-chip from Escherichia coli MG1655 K-12, WT and ∆arcA strains

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The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli [ChIP-Seq]

Project description:We found many binding sites for ArcA under glucose fermentative anaerobic growth conditions. Descirbed in the manuscript "The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli" Examination of occupancy of ArcA under anaerobic growth conditions.

2013-10-17 | E-GEOD-46414 | biostudies-arrayexpress

The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli [ChIP-Seq]

2013-10-17 | GSE46414 | GEO

ArcA Chip-chip from Escherichia coli MG1655 K-12, WT and M-bM-^HM-^FarcA strains

Project description:Mapping the occupancy of ArcA throughout the genome of Escherchia coli MG1655 K-12 using an affinity purified antibody under anaerobic and aerobic growth conditions. As a control, we also performed ChIP-chip onArcA in a M-bM-^HM-^FarcA mutant strain of Escherchia coli MG1655 K-12. Described in the manuscript The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli Mapping of occupancy of ArcA in the genome of Escherchia coli MG1655 K-12 during anaerobic fermentation and aerobic respiration. Immunoprecipitated DNA compared to INPUT for each sample.

2013-10-17 | E-GEOD-46413 | biostudies-arrayexpress

Expression analysis of Escherichia coli MG1655 K-12 WT and M-bM-^HM-^FarcA mutant

Project description:Investigation of whole genome gene expression level changes in a Escherichia coli MG1655 K-12 M-bM-^HM-^FarcA mutant, compared to the wild-type strain. The mutations engineered into this strain produce a strain lacking the ArcA protein. The results are further described in the manuscript The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli A six chip study using total RNA recovered from three separate cultures of Escherichia coli MG1655 K-12 WT and three separate cultures of the M-bM-^HM-^FarcA mutant strain. Each chip measures the expression level of 4,661 genes from Escherichia coli MG1655 K-12 with eight 60-mer probes per gene, with each probe represented twice on the array.

2013-10-17 | E-GEOD-46412 | biostudies-arrayexpress

The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli

Project description:The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli

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Thiol-Based Functional Mimicry of Phosphorylation of the Two-Component System Response Regulator ArcA Promotes Pathogenesis in Enteric Pathogens

Project description:Pathogenic bacteria can rapidly respond to stress environments, such as exposure to reactive oxygen species (ROS). The thiol (-SH) groups of cysteine residues in many proteins serve as redox-sensitive switches, providing triggers for ROS-mediated signaling events. In this study, we profiled the reversible thiol oxidation during ROS exposure of the proteome of Vibrio cholerae, a Gram-negative human pathogen that causes cholera. We identified posttranslational modifications of two cysteine residues of ArcA, a response regulator that is known to be phosphorylated under oxygen limiting conditions and regulates global carbon oxidation pathways. We showed that although ROS exposure abolished ArcA phosphorylation, it induced the formation of an intramolecular disulfide that promoted ArcA-ArcA interaction. Thiol oxidation of ArcA led to sustained ArcA activity and ROS resistance. We further demonstrated that V. cholerae ArcA cysteine residues were oxidized in cholera patient diarrheal stools, and that ArcA thiol oxidation is crucial for V. cholerae in vitro ROS resistance, colonization of ROS-rich gut niches, and environmental survival. Moreover, in other enteric pathogens such as Salmonella enterica, the cysteine residues in ArcA orthologs are conserved and thiol oxidation of ArcA plays important roles in ROS resistance both in vitro and in host cells. These results suggest that in enteric pathogens, as a response to ROS insults, thiol oxidation of ArcA is able to functionally mimic phosphorylation and retain ArcA activity, allowing for a balance in the expression of stress-related and pathogenesis-related genetic programs.

2021-08-02 | MSV000087932 | MassIVE

Escherichia coli str. K-12 substr. MG1655

Project description:ArcA Chip-chip from Escherichia coli MG1655 K-12, WT and ∆arcA strains

| PRJNA200300 | ENA

Fermentative and nitrate respiratory transcriptome analysis of E. coli K12 MG1655

Project description:Determining how facultative anaerobic organisms sense and direct cellular responses to electron acceptor availability has been a subject of intense study. However, even in the model organism Escherichia coli, established mechanisms only explain a small fraction of the hundreds of genes that are regulated during shifts in electron acceptor availability. Here we propose a qualitative model that accounts for the full breadth of regulated genes by detailing how two global transcription factors (TFs), ArcA and Fnr of E. coli, sense key metabolic redox ratios and act on a genome-wide basis to regulate anabolic, catabolic, and energy generation pathways. We first fill gaps in our knowledge of this transcriptional regulatory network by carrying out ChIP-chip and gene expression experiments to identify 463 regulatory events. We then interfaced this reconstructed regulatory network with a highly curated genome-scale metabolic model to show that ArcA and Fnr regulate > 80% of total metabolic flux and 96% of differential gene expression across fermentative and nitrate respiratory conditions. Finally, based on the data we propose a feedforward with feedback trim regulatory scheme by showing extensive repression of catabolic genes by ArcA and extensive activation of chemiosmotic genes by Fnr. We further corroborated this regulatory scheme by showing a 0.71 r2 (p < 1e-6) correlation between changes in metabolic flux and changes in regulatory activity across fermentative and nitrate respiratory conditions. We also are able to relate the proposed model to a wealth of previously generated data by contextualizing the existing transcriptional regulatory network.

2014-02-27 | GSE55365 | GEO

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