Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1086201 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28285170_1.fastq.gz | Fastqsanger.gz | |||
| SRR28285170_2.fastq.gz | Fastqsanger.gz | |||
| SRR28285171_1.fastq.gz | Fastqsanger.gz | |||
| SRR28285171_2.fastq.gz | Fastqsanger.gz | |||
| SRR28285172_1.fastq.gz | Fastqsanger.gz |
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Project description:Infections by the major opportunistic pathogen of human Candida albicans are commonly treated with echinocandin (ECN) drugs. However, C. albicans can adapt to grow in the presence of certain amounts of ECNs. Prior studies by several laboratories have defined multiple genes, as well as mechanisms involving induced aneuploidy, that can govern this. Still, mechanisms of ECN adaptation are not fully understood. Here, we use genome-wide profiling of chromatin accessibility by ATAC-seq to determine if ECN adaptation is reflected in changes in the chromatin landscape in the absence of aneuploidy. We find that drug adaptation is coupled with multiple changes in chromatin accessibility genome-wide, which occur predominantly in gene promoter regions. Areas of increased accessibilities in promoters are enriched with the binding motifs for at least two types of transcription factors: zipfinger and b-zipfinger. We also find that chromatin changes are often associated with differentially-expressed genes including genes with functions relevant to the ECN-adapted phenotype, such as cell wall biosynthesis. Consistent with this, we find that the cell wall is remodeled in ECN-adapted mutants, with chitin up and glucan down and increased cell surface exposure. Full understanding of ECN adaptation processes is of critical importance for prevention of clinical resistance.
2025-03-11 | GSE284528 | GEO
Project description:The Escherichia coli strain Nissle 1917 (EcN) is used as a probiotic for the treatment of certain gastrointestinal diseases in several European and non-European countries. In vitro studies showed EcN to efficiently inhibit the production of Shiga toxin (Stx) by Stx producing E. coli (STEC) such as Enterohemorrhagic E. coli (EHEC). The occurrence of the latest EHEC serotype (O104:H4) responsible for the great outbreak in 2011 in Germany was due to the infection of an enteroaggregative E. coli by a Stx 2-encoding lambdoid phage turning this E. coli into a lysogenic and subsequently into a Stx producing strain. Since EHEC infected persons are not recommended to be treated with antibiotics, EcN might be an alternative medication. However, because a harmless E. coli strain might be converted into a Stx-producer after becoming host to a stx encoding prophage, we tested EcN for stx-phage genome integration. Our experiments revealed the resistance of EcN towards not only stx-phages but also against the lambda phage. This resistance was not based on the lack of or by mutated phage receptors. Rather the expression of certain genes (superinfection exclusion B (sieB) and a phage repressor (pr) gene) of a defective prophage of EcN was involved in the complete resistance of EcN to infection by the stx- and lambda phage. Obviously, EcN cannot be turned into a Stx producer. Furthermore, we observed EcN to inactivate phages and thereby to protect E. coli K-12 strains against infection by stx- as well as lambda-phages. Inactivation of lambda-phages was due to binding of lambda-phages to LamB of EcN whereas inactivation of stx-phages was caused by a thermostable protein of EcN. These properties together with its ability to inhibit Stx production make EcN a good candidate for the prevention of illness caused by EHEC and probably for the treatment of already infected people.
2018-06-14 | GSE109932 | GEO
Project description:To build therapeutic strains, Escherichia coli Nissle (EcN) have been engineered to express antibiotics, toxin-degrading enzymes, immunoregulators, and anti-cancer chemotherapies. For efficacy, the recombinant genes need to be highly expressed, but this imposes a burden on the cell, and plasmids are difficult to maintain in the body. To address these problems, we have developed landing pads in the EcN genome and genetic circuits to control therapeutic gene expression. These tools were applied to EcN SYNB1618, undergoing clinical trials as a phenylketonuria treatment. The pathway for converting phenylalanine to trans-cinnamic acid was moved to a landing pad under the control of a circuit that keeps the pathway off during storage. The resulting strain (EcN SYN8784) achieved higher activity than EcN SYNB1618, reaching levels near when the pathway is carried on a plasmid. This work demonstrates a simple system for engineering EcN that aids quantitative strain design for therapeutics.
2023-05-15 | GSE228761 | GEO
Project description:To determine whether calprotectin can elicit any transcriptional response in the probiotic E. coli Nissle 1917(EcN), EcN was treated with 200 ug/g of calprotectin in log phase.
2023-08-16 | GSE211418 | GEO
Project description:Escherichia coli Nissle 1917 (EcN) is a probiotic used for treatment of intestinal disorders. EcN improves gastrointestinal homeostasis and microbiota balance; however little is known about how this probiotic delivers effector molecules to the host. Outer membrane vesicles (OMVs) are constitutively produced by gram-negative bacteria and have a relevant role in bacteria-host interactions. Here we performed proteomic analysis of EcN OMVs. Using 1D SDSD-PAGE and highly sensitive LC-MS/MS analysis we identified 192 EcN vesicular proteins with high confidence in three independent experiments. Of these proteins, 18 were encoded by strain-linked genes and 57 were common to pathogen-derived OMVs. These proteins may contribute to the ability of this probiotic to colonize the human gut as they fulfil functions related to adhesion to host tissues, immune modulation or bacterial survival in host niches. This study describes the first global OMV proteome of a probiotic strain and provides evidence that probiotic-derived OMVs contain proteins that can target these vesicles to the host and mediate their beneficial effects on intestinal function.
2013-12-19 | PXD000367 | Pride
Project description:A healthy rumen is crucial for normal growth and improved production performance of ruminant animals. Rumen microbes participate in and regulate rumen epithelial function, and the diverse metabolites produced by rumen microbes are important participants in rumen microbe-host interactions. SCFAs, as metabolites of rumen microbes, have been widely studied, and propionate and butyrate have been proven to promote rumen epithelial cell proliferation. Succinate, as an intermediate metabolite in the citric acid cycle, is a final product in the metabolism of certain rumen microbes, and is also an intermediate product in the microbial synthesis pathway of propionate. However, its effect on rumen microbes and rumen epithelial function has not been studied. It is unclear whether succinate can stimulate rumen epithelial development. Therefore, in this experiment, Chinese Tan sheep were used as experimental animals to conduct a comprehensive analysis of the rumen microbiota community structure and rumen epithelial transcriptome, to explore the role of adding succinate to the diet in the interaction between the rumen microbiota and host.
2023-06-12 | GSE233696 | GEO