Ontology highlight
ABSTRACT:
PROVIDER: PRJNA563564 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR10058900_1.fastq.gz | Fastqsanger.gz | |||
| SRR10058900_2.fastq.gz | Fastqsanger.gz | |||
| SRR10058901_1.fastq.gz | Fastqsanger.gz | |||
| SRR10058901_2.fastq.gz | Fastqsanger.gz |
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Project description:The mutagenicity of bacteria was assessed by serially exposing human small intestinal organoids to various bacterial species or isolated toxins.
We have used the following abbreviations:
EWT: Organoids exposed to E. coli described in PMID: 32106218
EKO: Organoids exposed to isogenic E. coli as EWT, with knockout of the deltaClbQ gene, rendering them unable to produce colibactin
DYE: Organoids exposed to FastGreen injection control dye
NIS: Organoids exposed to E. coli Nissle
ETBF: Organoids exposed to the protease toxin BTF produced by ETBF-bacteria.
| EGAD00001008687 | EGA
Project description:This experiment studied the effect of FPP accumulation on E. coli. E. coli cells transformed with pMBIS (the S. cerevisiae mevalonate pathway enzymes converting mevalonate to FPP) and fed mevalonate produce large amounts of FPP, which causes toxicity when it accumulates. When coupled with an active amorphadiene synthase (pADS) the cells produce amorphadiene, a non-toxic isoprenoid. To accumulate FPP, but maintain similar protein burden, an amorphadiene synthase with 3 mutations to render it inactive was used (pADSmut) to accumulate FPP. E. coli was transformed with pMBIS and pADS or pMBIS and pADSMut and grown in LB and fed 10 mM mevalonate and induced with 0.5 mM IPTG, then sampled at subsequent time points.
2011-05-13 | GSE29267 | GEO
Project description:This experiment studied the effect of FPP accumulation on E. coli. E. coli cells transformed with pMBIS (the S. cerevisiae mevalonate pathway enzymes converting mevalonate to FPP) and fed mevalonate produce large amounts of FPP, which causes toxicity when it accumulates. When coupled with an active amorphadiene synthase (pADS) the cells produce amorphadiene, a non-toxic isoprenoid. To accumulate FPP, but maintain similar protein burden, an amorphadiene synthase with 3 mutations to render it inactive was used (pADSmut) to accumulate FPP. E. coli was transformed with pMBIS and pADS or pMBIS and pADSMut and grown in M9+glucose with varying magnesium concentrations and fed 20 mM mevalonate and induced with 0.5 mM IPTG, then sampled at subsequent time points.
2011-07-07 | GSE30403 | GEO
Project description:Investigation of whole genome gene expression level changes in a Escherichia coli MG1655 K-12 ∆arcA mutant, compared to the wild-type strain. The mutations engineered into this strain produce a strain lacking the ArcA protein. The results are further described in the manuscript The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli
2013-10-17 | GSE46412 | GEO
Project description:mcr-1-encoding E. coli isolates from German pigs
| PRJEB21879 | ENA
Project description:Background: Members of E. coli serogroup O45 are porcine enteropathogenic E. coli (PEPEC) strains which cause post-weaning diarrhea and produce characteristic attaching and effacing (A/E) lesions. Most of O45 PEPEC strains possess the locus of enterocyte effacement (LEE), encoding the virulence factors for A/E lesions, and often possess the paa gene, which is thought to contribute to the early stages of PEPEC virulence. Methodology: Nine O45 PEPEC strains and a rabbit enteropathogenic (REPEC) strain, known to produce A/E lesions, were characterized using an E. coli O157-E. coli K12 whole genome microarray and a virulence gene-specific microarray, and by PCR experiments. Results: Based on their virulence genes profiles, the 10 strains were characterized as atypical EPEC. The differences in their genomes pointed to two distinct evolutionary groups of O45 PEPEC, Group I and Group II, and to the contribution these genetic differences have on virulence in pigs. Group I contained the REPEC strain and four O45 PEPEC strains known to induce severe A/E lesions in challenged pigs whereas Group II was composed of five other O45 PEPEC strains which induced less severe or no A/E lesions in challenged pigs. Significant differences between Groups I and II were found in the presence or absence of 50 O-Islands (OIs) or S-loops and 13 K-islands (KIs) or K-loops, including the virulence-associated islands OI#1 (S-loop#1), OI#47 (S-loop#71), OI#57 (S-loop#85), OI#71 (S-loop#108), OI#115, OI#122, and OI#154 (S-loop#253).
2009-07-11 | GSE17036 | GEO
Project description:Investigation of whole genome gene expression level changes in a Escherichia coli MG1655 K-12 ∆fnr mutant, compared to the wild-type strain. The mutations engineered into this strain produce a strain lacking the FNR protein.
2013-06-20 | GSE41190 | GEO
Project description:This experiment studied the effect of FPP accumulation on E. coli. E. coli cells transformed with pMBIS (the S. cerevisiae mevalonate pathway enzymes converting mevalonate to FPP) and fed mevalonate produce large amounts of FPP, which causes toxicity when it accumulates. When coupled with an active amorphadiene synthase (pADS) the cells produce amorphadiene, a non-toxic isoprenoid. To accumulate FPP, but maintain similar protein burden, an amorphadiene synthase with 3 mutations to render it inactive was used (pADSmut) to accumulate FPP. E. coli was transformed with pMBIS and pADS or pMBIS and pADSMut and grown in LB and fed 10 mM mevalonate and induced with 0.5 mM IPTG, then sampled at subsequent time points. This comparison is between E. coli DH1 cells accumulating FPP via the heterologous mevalonate pathway (pMBIS/pADSmut) to cells producing amorphadiene via the same pathway (pMBIS/pADS). Samples were collected 2.5, 5, 7, and 29.5 hr after addition of IPTG and mevalonate. One biological replicate was used. Total RNA was extracted, reverse transcribed, labeled, and hybridized to multiple slides for technical replicates.
2011-05-13 | E-GEOD-29267 | biostudies-arrayexpress