Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic study of E. coli 042 with a variant of aggR gene with a FRT sequence inserted in its 3´UTR by RNA-seq

ABSTRACT: Transcriptomic study of E. coli 042 with a variant of aggR gene with a FRT sequence inserted in its 3´UTR by RNA-seq

PROVIDER: PRJNA673214 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12937903.fastq.gz	Fastqsanger.gz
	SRR12937904.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Transcriptomic study of E. coli 042 with a variant of aggR gene with a FRT sequence inserted in its 3´UTR by RNA-seq

Project description:A common genomic feature of most EAEC strains is the presence of a virulence plasmid termed pAA. Plasmid-encoded virulence determinants are, among others, a transcriptional activator termed AggR, a member of the AraC-XylS family of transcription factors. We have previously determined the direct correlation between (p)ppGpp, expression of AggR and biofilm development in strain EAEC 042 (https://doi.org/10.3389/fmicb.2018.00717). In this work we characterize a novel variant of the aggR gene. We modified its 3´UTR by insertion of a FRT sequence, which have generated a series of different phenotypes. We used RNA-seq to compare the transcriptome of the wt strain and its aggR3UTRFRT variant grown at 37ºC in LB medium.

2021-10-29 | GSE160448 | GEO

Dominant MLH1 epimutation linked to 5'UTR variant c.-27C>A

Project description:Constitutional epimutations of tumor suppressor genes manifest as promoter methylation and transcriptional silencing of a single allele in normal somatic tissues, thereby predisposing to cancer. Constitutional MLH1 epimutations occur in individuals with young-onset cancer and demonstrate non-Mendelian inheritance through their reversal in the germline. We report a cancer-affected family showing dominant transmission of soma-wide highly mosaic MLH1 methylation and transcriptional repression linked to a particular genetic haplotype. The epimutation was erased in spermatozoa but reinstated in the somatic cells of the next generation. The affected haplotype harbored two single nucleotide substitutions in tandem: c.-27C>A located near the transcription initiation site and c.85G>T. The c.-27C>A variant significantly reduced transcriptional activity in reporter assays and is the probable cause of this epimutation. Five members of a three-generation Caucasian Lynch syndrome family with an autosomal dominant MLH1 epimutation linked to a single nucleotide variant (c.-27C>A) within the MLH1 5'UTR were examined for copy number variations and retention of heterozygosity on chromosome 3. These five carriers of constitutional MLH1 methylation and the c.-27C>A variant were compared with 300 healthy Caucasian controls from the Wellcome Trust Case Control Consortium using three algorithms (QuantiSNP, PennCNV, COKGEN) to detect any copy number variants. The five family members studied were female (the proband II5, her affected mother I1, and three asymptomatic relatives II2, II4 and III2) are labeled according to the pedigree in Figure 3 of the associated publication (Hitchins et al., Cancer Cell, 2011). The supplementary file 'GSE30348_gw6.lrr_baf.txt' contains log R ratio and B-allele frequency values in a tab-delimited format with one marker per row.

2011-07-01 | E-GEOD-30348 | biostudies-arrayexpress

Escherichia coli 042

Project description:Escherichia coli 042 genome sequencing project

| PRJEA40647 | ENA

NOD2 and desease associated variant NOD2-L1007fsinsC dependent genomewide transcriptional regulation in stable Flp-In HEK cells

Project description:NOD2 is an intracellular receptor for the bacterial cell wall component muramyl dipeptide (MDP) and variants of NOD2 are associated with chronic inflammatory diseases of barrier organs e.g. Crohn disease, asthma and atopic eczema. It is known that activation of NOD2 induces a variety of inflammatory and antibacterial factors. The exact transcriptomal signatures that define the cellular programs downstream of NOD2 activation and the influence of the Crohn-associated variant L1007fsinsC are yet to be defined. To describe the MDP-induced activation program, we analyzed the transcriptomal reactions of isogenic HEK293 cells expressing NOD2wt or NOD2L1007fsinsC to stimulation with MDP. Importantly, a clear loss-of-function could be observed in the cells carrying the Crohn-associated variant L1007fsinsC, while the NOD2wt cells showed differential regulation of growth factors, chemokines and several antagonists of NF-κB, e.g. TNFAIP3 (A20) and IER3. To elucidate the MDP-induced activation program we generated isogenic HEK293 cells stably expressing wildtype NOD2 or NOD2L1007fsinsC using a FRT-recombinase based approach. Cells carrying the inserted vector cassette were used as controls (mock-transfectant). To comprehensively analyze NOD2-mediated innate immune responses we analyzed transcriptomal signature patterns using genome-wide cDNA microarrays. Samples were harvested from cell cultures under normal growth conditions 0 h, 2 h and 6 h after MDP‑ stimulation of the cells.

2013-01-01 | E-GEOD-22611 | biostudies-arrayexpress

SynGAP variant from Japanese ALS cohort alters the recruitment of RNA binding proteins

Project description:FUS is one of the pathogenic RNA-binding proteins for amyotrophic lateral sclerosis (ALS). We previously reported that FUS stabilized SynGAP mRNA at its 3’UTR and maintained spine maturation and cognitive function in mice. To elucidate whether this mechanism could be pathogenic for ALS, we identified SynGAP 3’UTR variant at the binding site of FUS, different from that in mice, from a multicenter cohort in Japan. Human induced pluripotent stem cells (hiPSC)-derived motor neurons with SynGAP variant showed spine abnormality with aberrant SynGAP splicing. To evaluate how SynGAP variant altered the access of RNA binding proteins to SynGAP 3'UTR, we performed pull down assay by using biotinylated RNA probes with or without the variant.

2023-03-11 | PXD026586 | Pride

Enhydrobacter sp. JGI 042

Project description:Enhydrobacter sp. JGI 042 Genome sequencing

| PRJNA340617 | ENA

Marinobacter sp. es.042

Project description:Marinobacter sp. ES.042 genome sequencing

| PRJNA303381 | ENA

Epicoccum sp. 1-042

Project description:Epicoccum sp. 1-042 Genome sequencing and assembly

| PRJNA1030172 | ENA

Epicoccum sp. 1-042

Project description:Epicoccum sp. 1-042 Genome sequencing and assembly