RNA-seq analysis of isogenic dnaN+ and dnaN-E202K E. coli strains derived from MG1655.
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ABSTRACT:
ORGANISM(S): Escherichia coli
PROVIDER: GSE175936 | GEO | 2021/06/02
REPOSITORIES: GEO
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Project description:RNA-seq analysis of isogenic dnaN+ and dnaN-E202K E. coli strains derived from MG1655.
| PRJNA734325 | ENA
Project description:overexpressing DnaN did not affect the genomic DNA pattern in a strain that replicated form the plasmid origin of replication oriN and is deleted for the endogenous origin of replication oriC
2009-09-01 | GSE17809 | GEO
Project description:Overexpression of DnaN causes the accumulation of origin of replication proximal DNA.
2009-09-01 | GSE17808 | GEO
Project description:Abstract — Within the US military, new insensitive munitions (IMs) are rapidly replacing conventional munitions improving safety from unintended detonation. Toxicity data for IM chemicals are expanding rapidly, however IM constituents are typically deployed in mixture formulations, and very little is known about their mixture toxicology. In the present study we sought to characterize the mixture effects and toxicology of the two predominant IM formulations IMX-101 and IMX-104 in acute (48 h) larval fathead minnow (Pimephales promelas) exposures. IMX-101 consists of a mixture of 2,4-dinitroanisole (DNAN), 3-nitro-1,2,4-triazol-5-one (NTO), and nitroguanidine (NQ) while IMX-104 is composed of DNAN, NTO, and hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX). DNAN was the most potent constituent in IMX-101 eliciting an LC50 of 36.1 mg/L, whereas NTO and NQ did not elicit significant mortality in exposures up to 1040 and 2640 mg/L, respectively. Toxic unit calculations indicated that IMX-101 elicited toxicity representative of the component concentration of DNAN within the mixture. Toxicogenomic responses for the individual constituents of IMX-101 indicated unique transcriptional expression and functional responses characteristic of: oxidative stress, impaired energy metabolism, tissue damage and inflammatory responses in DNAN exposures; impaired steroid biosynthesis and developmental cell-signaling in NQ exposures; and altered mitogen-activated protein kinase signaling in NTO exposures. Transcriptional responses to the IMX-101 mixture were driven by the effects of DNAN where expression and functional responses were nearly identical comparing DNAN alone versus the fractional equivalent of DNAN within IMX-101. Given that each individual constituent of the IMX-101 mixture elicited unique functional responses, and NTO and NQ did not interact with DNAN within the IMX-101 mixture exposure, the overall toxicity and toxicogenomic responses within acute exposures to the IMX-101 formulation are indicative of "independent" mixture toxicology. Alternatively, in the IMX-104 exposure both DNAN and RDX were each present at concentrations sufficient to elicit lethality (RDX LC50 = 28.9 mg/L). Toxic-unit calculations for IMX-104 mixture formulation exposures indicated slight synergistic toxicity (ΣTU LC50 = 0.82, 95% confidence interval = 0.73-0.90). Unique functional responses relative to DNAN were observed in the IMX-104 exposure including responses characteristic of RDX exposure. Based on previous transcriptomics responses to acute RDX exposures in fathead minnow larvae, we hypothesize that the potentially synergistic responses within the IMX-104 mixture are related to interactive effects of each DNAN and RDX on oxidative stress mitigation pathways.
2018-03-01 | GSE101870 | GEO
Project description:Abstract - Current in vitro hazard assessment techniques lack the systems context necessary to holistically describe in vivo toxicity. To remedy this shortcoming, we have employed the Integrated discrete Multiple Organ Co-Culture (IdMOC) system in conjunction with global-transcriptomic expression assessment to provide a systems context of interactive organ and toxicity pathway responses. Specifically, IdMOC exposures containing human cells representative of five organ types (kidney, liver, lung, vascular endothelium and heart muscle) were compared to mono-culture exposures, to evaluate toxic effects in a well-studied legacy munition, 2,4,6-trinitrotoluene (TNT) compared to a structurally similar insensitive munition, 2,4-dinitroanisole (DNAN) having sparsely described toxicity. DNAN toxicity, based on cell viability, was significantly lower than TNT for three cell lines: liver, vascular endothelium, and heart. Toxicity pathways enriched in transcriptional analysis of kidney cells exposed to TNT and DNAN through the IdMOC system reflected the literature-based in vivo mammalian toxicity of parent compounds and metabolites where multiple screening values matched chronic dosing levels within 1 order of magnitude. Enriched pathways were primarily unique to each chemical where TNT exposures affected xenobiotic metabolism, oxidative stress, and cell cycle pathways in addition to pathways providing potential screening for hematotoxicity, renal toxicity and urinary cancer. Ten pathway-level responses from IdMOC suggested that DNAN elicited toxicity representative of the primary metabolite, 2,4-dinitrophenol (2,4-DNP). Relative to monoculture, IdMOC results provided a higher number and more robust enrichment of pathways involved in known in vivo toxicity mechanisms for TNT and a profile indicative of in vivo systemic toxicity of DNAN and metabolite 2,4-DNP.
2018-12-01 | GSE90617 | GEO
Project description:We used the soil nematode Caenorhabditis elegans, a well-characterized genomics model organism, as the test organism and a species-specific, genome-wide 44K-oligo probe microarray for gene expression analysis. Our goal was to discern toxicological mechanisms for three insensitive munitions formulation IMX-101 constituents 2,4-dinitroanisole (DNAN), nitroguanidine (NQ) and nitrotriazolone (NTO) at the molecular level.
2017-06-01 | GSE92365 | GEO
Project description:We built 3 strains from Candida albicans wild-type strains, mutant strain with one TRK1 gene deleted(one allele of two genes was deleted), overexpression strain(add one allele of the gene to rp10 locus), and restoration strain(add one allele of the gene to mutant strains). The goal is study the expression level change of genes among the three strains compared with wild-type strain on a genomic scale. Keywords: genetic modification
2007-07-18 | GSE8475 | GEO
Project description:To investigate the evolutionary divergence of transcriptional regulation between the mouse subspecies, we performed transcriptome analysis by microarray on testes from the X-chromosome substitution strain, which carries different subspecies-derived X chromosome on the host subspecies genome. Transcription profiling showed that large-scale aberrations in gene expression were occurred on the introgressed X chromosome. This improper expression was restored by introducing chromosome 1 from the same donor strain as the X chromosome, suggesting that the genetic incompatibility between trans-acting regulatory gene(s) on chromosome 1 and X-linked downstream genes might be a cause of the misregulation. Testes were collected from 5- and 7-day-old males for RNA extraction and the microarray experiments were performed by using Affymetrix microarrays. Testes from three different males for each strain were tested independently. Tested males are from control C57BL/6J (B6) strain, MSM strain, X-chromosome substitution strain (B6-ChrXMSM), partial X-chromosome substitution strain 1 (B6-ChrXTMSM), partial X-chromosome substitution strain 2 (XS39-tel), and restored (B6-ChrXTMSM X B6-Chr1MSM) F1.
2014-01-31 | E-GEOD-50687 | biostudies-arrayexpress
Project description:To compare transcriptional profiling of a gadE-, hdeA-, or hdeD- deficient strain to wild type in E. coli under minimum medium conditions. These genes are included in the GAD cluster genes, which are involved in the glutamic acid-dependent acid resistance (GAD) in E. coli. Goal was to determine the GadE, HdeA, or HdeD regulon in E. coli. Biological replicates: 2 replicates.
2021-06-27 | GSE178954 | GEO
Project description:With the goal of solving the whole-cell problem with Escherichia coli K-12 as a model cell, highly accurate genomes were determined for two closely related K-12 strains, MG1655 and W3110. Completion of the W3110 genome and comparison with the MG1655 genome revealed differences at 267 sites, including 251 sites with short, mostly single-nucleotide, insertions or deletions (indels) or base substitutions (totaling 358 nucleotides), in addition to 13 sites with an insertion sequence element or defective prophage in only one strain and two sites for the W3110 inversion. Direct DNA sequencing of PCR products for the 251 regions with short indel and base disparities revealed that only eight sites are true differences. The other 243 discrepancies were due to errors in the original MG1655 sequence, including 79 frameshifts, one amino-acid residue deletion, five amino-acid residue insertions, 73 missense, and 17 silent changes within coding regions. Errors in the original MG1655 sequence (<1 per 13,000 bases) were mostly within portions sequenced with out-dated technology based on radioactive chemistry.
| S-EPMC1681481 | biostudies-literature