Acetobacter ghanensis strain:JN01
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ABSTRACT:
PROVIDER: PRJNA1265713 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Complete genome sequence of Acetobacter ghanensis
| PRJEB7123 | ENA
Project description:Acetobacter ghanensis DSM 18895 genome sequencing project
| PRJDB1014 | ENA
Project description:Acetic acid bacteria are obligately aerobic alphaproteobacteria that have a unique ability to incompletely oxidize various alcohols and sugars to organic acids. The ability of these bacteria to incompletely oxidize ethanol to acetate has been historically utilized for vinegar production. The mechanism of switching between incomplete oxidation and assimilatory oxidation and the control of energy and carbon metabolism in acetic acid bacteria are not fully understood. To understand the physiology and molecular biology of acetic acid bacteria better, we determined the draft genome sequence of Acetobacter aceti NBRC 14818, which is the type strain of the genus. Based on this draft genome sequence, the transcriptome profiles in A. aceti cells grown on ethanol, acetate, glucose, or mix of ethanol and glucose was determined by using NimbleGen Prokaryotic Expression array (4x72K).
2011-01-17 | GSE24361 | GEO
Project description:Acetic acid bacteria are obligately aerobic alphaproteobacteria that have a unique ability to incompletely oxidize various alcohols and sugars to organic acids. The ability of these bacteria to incompletely oxidize ethanol to acetate has been historically utilized for vinegar production. The mechanism of switching between incomplete oxidation and assimilatory oxidation and the control of energy and carbon metabolism in acetic acid bacteria are not fully understood. To understand the physiology and molecular biology of acetic acid bacteria better, we determined the draft genome sequence of Acetobacter aceti NBRC 14818, which is the type strain of the genus. Based on this draft genome sequence, the transcriptome profiles in A. aceti cells grown on ethanol, acetate, glucose, or mix of ethanol and glucose was determined by using NimbleGen Prokaryotic Expression array (4x72K). Acetobacter aceti NBRC14818 was cultivated in the medium containing ethanol, acetate, glucose, or mix of ethanol and glucose as carbon sources in Erlenmeyer flask with rotary shaking. Total RNA was extracted when optical density at 600 nm was 0.3-0.4. The experiment was performed in duplicate independent cultures.
2011-01-17 | E-GEOD-24361 | biostudies-arrayexpress
Project description:Time-dependent transcriptome change in the A. aceti cells during growth on ethanol was determined by NimbleGen Eukaryotic Expression array (4x72K). Acetobacter aceti NBRC14818 was cultivated in the medium containing ethanol in Erlenmeyer flask with rotary shaking. Total RNA was extracted when optical density at 600 nm was 0.1, 0.2, 0.6, or 1.2. The experiment was performed in duplicate independent cultures.
2012-01-31 | E-GEOD-31597 | biostudies-arrayexpress
Project description:Trascriptome profiles in the cells of A. aceti wild-type strain and its isogenic aceA glcB mutant during growth in medium contaning ethanol and glucose was determined by NimbleGen Eukaryotic Expression array (4x72K). Acetobacter aceti NBRC14818 and its isogenic aceA glcB mutant were cultivated in medium containing ethanol and glucose in Erlenmeyer flask with rotary shaking. Total RNA was extracted when optical density at 600 nm was 0.3. The experiment was performed in duplicate independent cultures.
2012-11-30 | E-GEOD-38524 | biostudies-arrayexpress
Project description:MCF12A monolayer cultures were exposed to ethanol or acetaldehyde for eiher 1 week or 4 weeks Total RNA samples were assayed for gene expression and for microRNA expression. MicroRNA expression was accomplished using 2 experiments. The first experiment included untreated control, ethanol treated (4 weeks at 2.5 mM) and acetaldehyde treated (4 weeks at 1 mM). The data are presented in order of control1 for the ethanol and acetaldehyde treated samples followed by the ethanol and acetaldehyde treated samples, and then the control2 for the soft agar selected sample followed by the soft agar selected sample. The microRNA names are included in separate columns.
2017-02-10 | GSE76952 | GEO
Project description:Alcoholism is associated with breast cancer incidence and progression, and moderate chronic consumption of ethanol is a risk factor. The mechanisms involved in alcohol's oncogenic effects are unknown, but it has been speculated that they may be mediated by acetaldehyde. Here, we use the immortalized normal human epithelial breast cell line MCF-12A to determine whether short- or long-term exposure to ethanol or to acetaldehyde, using in vivo compatible ethanol concentrations, induces their oncogenic transformation and/or the acquisition of epithelial mesenchymal transition (EMT). Cultures of MCF-12A cells were incubated with 25 mM ethanol or 2.5 mM acetaldehyde for 1 week, or with lower concentrations (1.0-2.5 mM for ethanol, 1.0 mM for acetaldehyde) for 4 weeks. In the 4 wk incubation, cells were also tested for anchorage independence, including isolation of soft agar selected cells (SASC) from the 2.5 mM ethanol incubations. Cells were analyzed by immuno-cytofluorescence, flow cytometry, western blotting, DNA microarrays, RT/PCR, and assays for miRs. We found that short-term exposure to ethanol, but not, in general, to acetaldehyde, was associated with transcriptional upregulation of the metallothionein family genes, alcohol metabolism genes, and genes suggesting the initiation of EMT, but without related phenotypic changes. Long-term exposure to the lower concentrations of ethanol or acetaldehyde induced frank EMT changes in the monolayer cultures and in SASC as demonstrated by changes in cellular phenotype and mRNA expression. This suggests that low concentrations of ethanol, with little or no mediation by acetaldehyde, induce EMT and some traits of oncogenic transformation such as anchorage independence in normal breast epithelial cells. MCF12A monolayer cultures were exposed to ethanol or acetaldehyde for either 1 week or 4 weeks. Total RNA samples were assayed for gene expression and for microRNA expression.
2017-02-10 | GSE76951 | GEO
Project description:Alcoholism is associated with breast cancer incidence and progression, and moderate chronic consumption of ethanol is a risk factor. The mechanisms involved in alcohol's oncogenic effects are unknown, but it has been speculated that they may be mediated by acetaldehyde. Here, we use the immortalized normal human epithelial breast cell line MCF-12A to determine whether short- or long-term exposure to ethanol or to acetaldehyde, using in vivo compatible ethanol concentrations, induces their oncogenic transformation and/or the acquisition of epithelial mesenchymal transition (EMT). Cultures of MCF-12A cells were incubated with 25 mM ethanol or 2.5 mM acetaldehyde for 1 week, or with lower concentrations (1.0-2.5 mM for ethanol, 1.0 mM for acetaldehyde) for 4 weeks. In the 4 wk incubation, cells were also tested for anchorage independence, including isolation of soft agar selected cells (SASC) from the 2.5 mM ethanol incubations. Cells were analyzed by immuno-cytofluorescence, flow cytometry, western blotting, DNA microarrays, RT/PCR, and assays for miRs. We found that short-term exposure to ethanol, but not, in general, to acetaldehyde, was associated with transcriptional upregulation of the metallothionein family genes, alcohol metabolism genes, and genes suggesting the initiation of EMT, but without related phenotypic changes. Long-term exposure to the lower concentrations of ethanol or acetaldehyde induced frank EMT changes in the monolayer cultures and in SASC as demonstrated by changes in cellular phenotype and mRNA expression. This suggests that low concentrations of ethanol, with little or no mediation by acetaldehyde, induce EMT and some traits of oncogenic transformation such as anchorage independence in normal breast epithelial cells. MCF12A monolayer cultures were exposed to ethanol or acetaldehyde for either 1 week or 4 weeks. Total RNA samples were assayed for gene expression and for microRNA expression.
2017-02-10 | GSE76950 | GEO