Ontology highlight
ABSTRACT:
PROVIDER: PRJNA855139 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20019018_1.fastq.gz | Fastqsanger.gz | |||
| SRR20019018_2.fastq.gz | Fastqsanger.gz | |||
| SRR20019019_1.fastq.gz | Fastqsanger.gz | |||
| SRR20019019_2.fastq.gz | Fastqsanger.gz | |||
| SRR20019020_1.fastq.gz | Fastqsanger.gz |
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Project description:The function of cvpA, a bacterial gene predicted to encode an inner membrane protein, is largely unknown. Early studies in E. coli linked cvpA to Colicin V secretion and recent work revealed that it is required for robust intestinal colonization by diverse enteric pathogens. In enterohemorrhagic E. coli (EHEC), cvpA is required for resistance to the bile salt deoxycholate (DOC). Here, we carried out genome-scale transposon-insertion mutagenesis and spontaneous suppressor analysis to uncover cvpA’s genetic interactions and identify common pathways that rescue the sensitivity of a ∆cvpA EHEC mutant to DOC. These screens demonstrated that mutations predicted to activate the σE-mediated extracytoplasmic stress response bypass the ∆cvpA mutant’s susceptibility to DOC. Consistent with this idea, we found that deletions in rseA and msbB and direct overexpression of rpoE restored DOC resistance to the ∆cvpA mutant. Analysis of the distribution of CvpA homologs revealed that this inner membrane protein is conserved across diverse bacterial phyla, in both enteric and non-enteric bacteria that are not exposed to bile. Together, our findings suggest that CvpA plays a role in cell envelope homeostasis in response to DOC and similar stress stimuli in diverse bacteria.
2020-12-01 | GSE162346 | GEO
Project description:Using Fourier transform ion cyclotron resonance mass spectrometry (FTICR-MS) on microcosm samples from early phase plant litter degradation, we found that proteins and condensed hydrocarbons are the compounds with the strongest correlation to dissolved organic carbon (DOC) concentration. Proteins correlated positively with DOC concentration, while tannins and condensed hydrocarbons correlated negatively with DOC. With nuclear magnetic resonance (NMR) spectroscopy, we identified 15 individual compounds associated with DOC concentration. Through random forest, neural network, and indicator species analyses, we identified bacterial and fungal taxa associated with DOC concentration and additionally identified connections between microorganisms and DOC chemical composition.
| MSV000088109 | MassIVE
Project description:C. jejuni, a spiral-shaped gram-negative bacterium, is a leading bacterial cause of human foodborne illness. Acute disease is associated with C. jejuni invasion of the intestinal epithelium. Further, maximal host cell invasion requires the secretion of proteins termed Campylobacter invasion antigens (Cia). As bile acids are known to alter the pathogenic behavior of other gastrointestinal pathogens, we hypothesized that the virulence potential of Campylobacter may be triggered by the bile acid deoxycholate (DOC). In support of this hypothesis, culturing C. jejuni with a physiologically relevant concentration of DOC significantly altered the kinetics of cell invasion as evidenced by gentamicin-protection assays. In contrast to C. jejuni harvested from Mueller-Hinton (MH) agar plates, C. jejuni harvested from MH agar plates supplemented with DOC demonstrated Cia secretion as judged by metabolic labeling experiments. DOC was also found to induce the expression of the ciaB gene as judged by B-galactosidase reporter assays and real-time RT-PCR. Microarray analysis revealed that DOC induced the expression of virulence genes (i.e., ciaB, cmeABC, dccR, and tlyA). In summary, we demonstrate that it is possible to enhance the pathogenic behavior of C. jejuni by modifying the culture conditions. These results provide a foundation to identify genes expressed by C. jejuni in response to in vivo-like culture conditions. Keywords: Stress response
2008-01-10 | GSE10110 | GEO
Project description:Linking bacterial community composition with bacterial DOC degradation
| PRJNA193478 | ENA
Project description:Kelp are the largest photosynthetic organisms in the ocean with tissue differentiation and complex life cycles. Other multicellular organisms with similar complexity such as plants and animals are well known to posses epigenetic mechanisms such as DNA methylation to control development and morphogenesis. Despite plant-like body plans and the presence of different life-cycle stages, the kelp species Saccharina japonica has only a very low level of DNA methylation, yet we have found strong evidence for differential methylation of regulatory elements and protein-coding genes which seem to contribute to the formation of life-cycle stages, tissue differentiation, growth and halogen metabolism. Thus, DNA methylation seems to play an important role in kelp, which has not been reported before.
2018-07-17 | GSE117191 | GEO
Project description:Estrogen clearly prevents osteoporotic bone loss by attenuating bone resorption. The molecular basis of how this is accomplished, however, remains elusive. Here we report a critical role of osteoclastic ERa in mediating estrogen action on bone in females. We selectively ablated ERa in differentiated osteoclasts (ERa dOc/dOc). ERa dOc/dOc females, but not males, exhibited clear trabecular bone loss, similar to the osteoporotic bone phenotype in post-menopausal women. Recovery of bone loss by estrogen treatment of the ovariectomized ERa dOc/dOc females was ineffective in the trabecular areas of the long bones and lumbar vertebral bodies. Osteoclastic apoptosis, induced by estrogen, occurred simultaneously with up-regulation of Fas ligand (FasL) expression in intact trabecular bones of ERa +/+mice, but not in ERa dOc/dOc mice. ERa was also required for similar effects of estrogen and tamoxifen in cultured osteoclasts. These findings suggest that the osteoprotective actions of estrogen and SERMS are mediated at least in part through osteoclastic ERa in trabecular bone; and the life span of mature osteoclasts is regulated through activation of the Fas/FasL system. Keywords: Study about estrogen response of osteoclast-specific estrogen receptor alpha mice
2007-06-01 | GSE7798 | GEO
Project description:Campylobacter jejuni is a major cause of food-borne gastroenteritis. Proteomics by label-based two-dimensional liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS) identified proteins associated with growth in 0.1% sodium deoxycholate (DOC, a component of gut bile salts), and system-wide validation was performed by data-independent acquisition (DIA-SWATH-MS). Proteins involved in nutrient transport were altered by DOC and aligned with intracellular changes to their respective carbon sources. DOC increased intracellular levels of sulfur-containing amino acids (cysteine and methionine) and the dipeptide cystine (Cys-Cys). A DOC induced transport protein was Cj0025c, which has sequence similarity to bacterial Cys-Cys transporters. Deletion of cj0025c (Δcj0025c) resulted in proteome changes consistent with sulfur starvation.
2020-05-08 | PXD017934 | Pride
Project description:C. jejuni, a spiral-shaped gram-negative bacterium, is a leading bacterial cause of human foodborne illness. Acute disease is associated with C. jejuni invasion of the intestinal epithelium. Further, maximal host cell invasion requires the secretion of proteins termed Campylobacter invasion antigens (Cia). As bile acids are known to alter the pathogenic behavior of other gastrointestinal pathogens, we hypothesized that the virulence potential of Campylobacter may be triggered by the bile acid deoxycholate (DOC). In support of this hypothesis, culturing C. jejuni with a physiologically relevant concentration of DOC significantly altered the kinetics of cell invasion as evidenced by gentamicin-protection assays. In contrast to C. jejuni harvested from Mueller-Hinton (MH) agar plates, C. jejuni harvested from MH agar plates supplemented with DOC demonstrated Cia secretion as judged by metabolic labeling experiments. DOC was also found to induce the expression of the ciaB gene as judged by B-galactosidase reporter assays and real-time RT-PCR. Microarray analysis revealed that DOC induced the expression of virulence genes (i.e., ciaB, cmeABC, dccR, and tlyA). In summary, we demonstrate that it is possible to enhance the pathogenic behavior of C. jejuni by modifying the culture conditions. These results provide a foundation to identify genes expressed by C. jejuni in response to in vivo-like culture conditions. Keywords: Stress response For the expression profiling arrays, an indirect comparison of gene expression was performed, where the expression profile of the C. jejuni F38011 cultured in the presence and absence of DOC was measured separately on different slides as described previously (26). Briefly, Cy5 labeled reference DNA from the C. jejuni F38011 strain was mixed with Cy3 labeled test cDNA (C. jejuni F38011 cultured in the presence or absence of DOC) and hybridized to the Campylobacter cDNA array (26) on separate slides. DNA microarrays were scanned using an Axon GenePix 4000B microarray laser scanner (Axon Instruments, Union City, CA) and the data for spot and background intensities were processed using the GenePix 4.0 software. To compensate for any effect of the amount of template and uneven Cy-dye incorporation, data normalization was performed as previously described (26). For the comparison of genes differentially expressed in the presence and absence of DOC,six hybridization measurements were generated per biological experiment (three technical replicate arrays and two replicate features per array).
2010-05-26 | E-GEOD-10110 | biostudies-arrayexpress
Project description:Genome wide gene expression analysis of mRNA siolated from whole heart tissue from wild type and cardiomyocyte selective MR null mice. The role of mineralocorticoid receptors (MR) in specific cell types of the myocardium in cardiac remodeling remains unknown. We investigated MR in cardiomyocytes in DOC/salt-induced cardiac pathology. Cardiomyocyte MR-null mice (CM-MRKO) and control mice (WT) were given DOC/salt and cardiac responses were examined at 8 days and 8 weeks. Cardiac function in untreated mice wild type and CM-MRKO mice was determined by Langendorf and showed no differences. At 8 days CM-MRKO showed equivalent monocyte/macrophage recruitment to wild type mice in response to DOC/salt treatment. Profibrotic markers were significantly reduced in CM-MRKO hearts at base line and in response to DOC/salt. In contrast, at 8 weeks CM-MRKO mice showed no DOC/salt-induced increase in inflammatory cell infiltrate, fibrosis or systolic blood pressure (SBP). Similarly, DOC/salt-mediated increases in proinflammatory and profibrotic gene expression were not detected in CM-MRKO mice. Although mRNA levels for fibronectin and collagen III were similar for each genotype, this was not translated into protein expression. Interestingly, untreated CM-MRKO mice showed increased mRNA and protein for decorin and a further increase with DOC/salt. Together, these data suggest a direct role for cardiomyocyte MR in DOC/salt-induced tissue remodelling and SBP regulation. Moreover, a specific profibrotic pathway is dysregulated in CM-MRKO mice, suggesting a potential mechanism for the cardioprotective effects of selective MR deletion in cardiomyocytes.
2013-06-30 | GSE38869 | GEO