Ethanol-producing bacteria
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1254750 | ENA |
REPOSITORIES: ENA
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Project description:Antimicrobial-producing soil bacteria isolated by Ouachita Baptist University students
| PRJNA554317 | ENA
Project description:The molecular mechanisms of ethanol toxicity and tolerance in bacteria, while important for biotechnology and bioenergy applications, remain incompletely understood. Genetic studies have identified potential cellular targets for ethanol and revealed multiple mechanisms of tolerance, but it remains difficult to separate direct and indirect effects of ethanol. We used adaptive evolution to generate spontaneous ethanol-tolerant strains of Escherichia coli, then characterized the mechanisms of toxicity and resistance associated with select mutations. Evolved alleles of metJ, rho, and rpsQ were sufficient to recapitulate much of the observed ethanol tolerance, implicating translation and transcription as key processes affected by ethanol. We found that ethanol induces mistranslation errors during protein synthesis, and that the evolved rpsQ allele protects cells by rendering the ribosome hyper-accurate. Ribosome profiling and RNAseq analyses of the ethanol-tolerant strain versus the wild type established that ethanol negatively affects transcriptional and translational processivity. Ethanol-stressed cells exhibited ribosomal stalling at internal AUG codons, which may be ameliorated by the adaptive inactivation of the MetJ repressor of methionine biosynthesis genes. Ethanol also caused aberrant intragenic transcription termination for mRNAs with low ribosome density, which was reduced in a strain with the adaptive rho mutation. Furthermore, ethanol inhibited transcript elongation by RNA polymerase in vitro. We propose that ethanol-induced inhibition and uncoupling of mRNA and protein synthesis are major contributors to ethanol toxicity in E. coli, and that adaptive mutations in metJ, rho, and rpsQ protect central dogma processes in the presence of ethanol.
2014-06-18 | GSE56372 | GEO
Project description:The molecular mechanisms of ethanol toxicity and tolerance in bacteria, while important for biotechnology and bioenergy applications, remain incompletely understood. Genetic studies have identified potential cellular targets for ethanol and revealed multiple mechanisms of tolerance, but it remains difficult to separate direct and indirect effects of ethanol. We used adaptive evolution to generate spontaneous ethanol-tolerant strains of Escherichia coli, then characterized the mechanisms of toxicity and resistance associated with select mutations. Evolved alleles of metJ, rho, and rpsQ were sufficient to recapitulate much of the observed ethanol tolerance, implicating translation and transcription as key processes affected by ethanol. We found that ethanol induces mistranslation errors during protein synthesis, and that the evolved rpsQ allele protects cells by rendering the ribosome hyper-accurate. Ribosome profiling and RNAseq analyses of the ethanol-tolerant strain versus the wild type established that ethanol negatively affects transcriptional and translational processivity. Ethanol-stressed cells exhibited ribosomal stalling at internal AUG codons, which may be ameliorated by the adaptive inactivation of the MetJ repressor of methionine biosynthesis genes. Ethanol also caused aberrant intragenic transcription termination for mRNAs with low ribosome density, which was reduced in a strain with the adaptive rho mutation. Furthermore, ethanol inhibited transcript elongation by RNA polymerase in vitro. We propose that ethanol-induced inhibition and uncoupling of mRNA and protein synthesis are major contributors to ethanol toxicity in E. coli, and that adaptive mutations in metJ, rho, and rpsQ protect central dogma processes in the presence of ethanol.
2014-06-18 | GSE56407 | GEO
Project description:Genome sequencing of bacteria isolated from patients with severe infectious diseases
| PRJDB16316 | ENA
Project description:The molecular mechanisms of ethanol toxicity and tolerance in bacteria, while important for biotechnology and bioenergy applications, remain incompletely understood. Genetic studies have identified potential cellular targets for ethanol and revealed multiple mechanisms of tolerance, but it remains difficult to separate direct and indirect effects of ethanol. We used adaptive evolution to generate spontaneous ethanol-tolerant strains of Escherichia coli, then characterized the mechanisms of toxicity and resistance associated with select mutations. Evolved alleles of metJ, rho, and rpsQ were sufficient to recapitulate much of the observed ethanol tolerance, implicating translation and transcription as key processes affected by ethanol. We found that ethanol induces mistranslation errors during protein synthesis, and that the evolved rpsQ allele protects cells by rendering the ribosome hyper-accurate. Ribosome profiling and RNAseq analyses of the ethanol-tolerant strain versus the wild type established that ethanol negatively affects transcriptional and translational processivity. Ethanol-stressed cells exhibited ribosomal stalling at internal AUG codons, which may be ameliorated by the adaptive inactivation of the MetJ repressor of methionine biosynthesis genes. Ethanol also caused aberrant intragenic transcription termination for mRNAs with low ribosome density, which was reduced in a strain with the adaptive rho mutation. Furthermore, ethanol inhibited transcript elongation by RNA polymerase in vitro. We propose that ethanol-induced inhibition and uncoupling of mRNA and protein synthesis are major contributors to ethanol toxicity in E. coli, and that adaptive mutations in metJ, rho, and rpsQ protect central dogma processes in the presence of ethanol. RNA-seq comparison of wild-type and mutant strains to assess readthrough of Rho-dependent transcriptional terminators
2014-06-18 | E-GEOD-56407 | biostudies-arrayexpress
Project description:The molecular mechanisms of ethanol toxicity and tolerance in bacteria, while important for biotechnology and bioenergy applications, remain incompletely understood. Genetic studies have identified potential cellular targets for ethanol and revealed multiple mechanisms of tolerance, but it remains difficult to separate direct and indirect effects of ethanol. We used adaptive evolution to generate spontaneous ethanol-tolerant strains of Escherichia coli, then characterized the mechanisms of toxicity and resistance associated with select mutations. Evolved alleles of metJ, rho, and rpsQ were sufficient to recapitulate much of the observed ethanol tolerance, implicating translation and transcription as key processes affected by ethanol. We found that ethanol induces mistranslation errors during protein synthesis, and that the evolved rpsQ allele protects cells by rendering the ribosome hyper-accurate. Ribosome profiling and RNAseq analyses of the ethanol-tolerant strain versus the wild type established that ethanol negatively affects transcriptional and translational processivity. Ethanol-stressed cells exhibited ribosomal stalling at internal AUG codons, which may be ameliorated by the adaptive inactivation of the MetJ repressor of methionine biosynthesis genes. Ethanol also caused aberrant intragenic transcription termination for mRNAs with low ribosome density, which was reduced in a strain with the adaptive rho mutation. Furthermore, ethanol inhibited transcript elongation by RNA polymerase in vitro. We propose that ethanol-induced inhibition and uncoupling of mRNA and protein synthesis are major contributors to ethanol toxicity in E. coli, and that adaptive mutations in metJ, rho, and rpsQ protect central dogma processes in the presence of ethanol. Examination of wild-type and mutant strains at three different time points (one pre-ethanol-stress, two post-ethanol-stress)
2014-06-18 | E-GEOD-56372 | biostudies-arrayexpress
Project description:Pseudomonas aeruginosa is an opportunistic pathogen frequently isolated from co-infections with Candida albicans and other ethanol-producing organisms. We found that ethanol, including that produced by C. albicans, stimulates the PhoB regulon in P. aeruginosa. We identify a subset of PhoB-regulated genes as differentially expressed in response to ethanol which are slightly different than the set of genes with increased expression in a genetically induced low phosphate response via pstB mutation.
2022-12-06 | GSE192694 | GEO
Project description:we used a label free quantitative proteomics approach, to describe the changes of protein expressions in C. reinhardtii and cobalamin producing bacteria Sinorhizobium meliloti 1021, in their interactions under different temperatures.
2022-05-25 | PXD032709 |
Project description:Purpose: The goals of this study are to use NGS-derived liver transcriptome profiling (RNA-seq) and identify differentially expressed genes in damaged livers that were exposed to 5% ethanol-containing liquid diet and ethanol binge. Methods: Liver mRNA profiles were generated from chronic ethanol feeding plus a single binge by deep sequencing, in duplicate, using Illumina Hiseq2500. qRT–PCR validation was performed using SYBR Green assay. Results: Chronic ethanol feeding plus a single binge treatment was associated with 422 downregulated genes and 384 upregulated genes, whereas Yap1 null livers had 351 downregulated genes and 287 upregulated genes after ethanol/CCl4 induced liver damage. Conclusions: This study provides detailed analysis of liver transcriptomes during hepatocyte damage caused by chronic ethanol feeding plus a single binge treatment, with biologic replicates, generated by RNA-seq technology.
2022-02-10 | GSE196314 | GEO
Project description:Whole genome sequencing of an ethanol-producing Bacillus amyloliquefaciens strain Jxnu-18
| PRJEB23600 | ENA