Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TrapSeq: An RNA Sequencing-based pipeline for the identification of genetrap insertions in mammalian cells

ABSTRACT: Current pipelines used to map genetrap insertion sites are based on inverse- or splinkerette-PCR methods, which despite their efficacy are prone to artifacts and do not provide information on the impact of the genetrap on the expression of the targeted gene. We developed a new method, which we named TrapSeq, for the mapping of genetrap insertions based on paired-end RNA sequencing. By recognizing chimeric mRNAs containing genetrap sequences spliced to an endogenous exon, our method identifies insertions that lead to productive trapping.

ORGANISM(S): Homo sapiens

PROVIDER: GSE99483 | GEO | 2018/02/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

TrapSeq: An RNA Sequencing-Based Pipeline for the Identification of Gene-Trap Insertions in Mammalian Cells.

Project description: Not available

| S-EPMC5695663 | biostudies-literature

Homo sapiens

Project description:TrapSeq: An RNA Sequencing-based pipeline for the identification of genetrap insertions in mammalian cells

| PRJNA388635 | ENA

pipeline metagenome

Project description:corroded pipelines Genome sequencing and assembly

| PRJNA387068 | ENA

Mechanisms of insertions at a double strand break

Project description:Insertions and deletions (indels) are common sources of structural variation, and insertions originating from spontaneous DNA lesions are frequent in cancer. We developed a highly sensitive assay (Indel-Seq) to monitor rearrangements in human cells at the TRIM37 acceptor locus that reports indels stemming from experimentallyinduced and spontaneous genome instability. Templated insertions, which derive from sequences genome-wide, require contact between donor and acceptor loci, homologous recombination, and are stimulated by DNA end-processing. Insertions are facilitated by transcription and involve a DNA/RNA hybrid intermediate. Indel-Seq reveals that insertions are generated via multiple pathways. The broken acceptor site anneals with a resected DNA break or invades the displaced strand of a transcription bubble or R-loop followed by DNA synthesis, displacement and then ligation by nonhomologous end-joining. Our studies identify transcription-coupled insertions as a critical source of spontaneous genome instability that are distinct from cut-and-paste events

2023-07-03 | GSE234089 | GEO

Detection of unbalanced insertions by aCGH and FISH

Project description:Insertions occur when a segment of one chromosome is translocated and inserted into a new region of the same chromosome or a non-homologous chromosome. We report 69 cases with unbalanced insertions identified using array CGH and FISH, representing 1.25% of 5,683 cases referred to our laboratory for array CGH and found to have copy-number abnormalities. Although the majority of insertions were non-recurrent, several recurrent unbalanced insertions were detected, including three der(Y)ins(Y;18)(q?11.2;p11.32p11.32)pat inherited from parents carrying an unbalanced insertion. The clinical significance of these recurrent rearrangements is unclear, although the small size, limited gene content, and inheritance pattern of each suggests the phenotypic consequences may be benign. Moreover, cryptic, submicroscopic duplications were observed at or near the insertion sites in two patients, further confounding the clinical interpretation of these insertions. Using FISH, linear amplification and array CGH we identified a 126-kb duplicated region from 19p13.3 inserted into MECP2 at Xq28 in a patient with symptoms of Rett syndrome. Our results demonstrate that although the interpretation of most non-recurrent insertions is unclear without high-resolution insertion site characterization, the potential for an otherwise benign duplication to result in a clinically relevant outcome through the disruption of a gene necessitates the use of FISH to determine whether copy-number gains detected by array CGH represent tandem duplications or unbalanced insertions. Further follow-up testing using techniques such as linear amplification coupled with array CGH or sequencing should be used to determine gene involvement at the insertion site after FISH has identified the presence of an insertion. 88 total samples analyzed. No replicates included. Each sample run against a standard sex-matched control.

2011-02-28 | E-GEOD-27080 | biostudies-arrayexpress

MATT mapping of Transposon insertions sites of strain G27 GPS-cat library

Project description:Genomic DNA from pools of H. pylori strain G27 Clones as indicated (pools of 300 (300p) or insertions in specific mapped genes) were amplifed using the MATT method to label DNA adjacent to the site of transposon insertion with the primer pairs indicated. The left side of the transposon was labeled in the Cy3 channel (Primer S) and the right side of the transposon was labeled in the Cy5 channel (Primer N). Computed

2005-08-26 | E-GEOD-3197 | biostudies-arrayexpress

KBM7 genetrap mutant cells stimulated with TNF-alpha and IFN-gamma

Project description:Transcriptional response of KBM7 cells to IFN-gamma or TNF-alpha was investigated in control or cells with genetrap insertions in JAK2 or TNFRS1A, respectively. The experiment shows that, as expected, cells lacking JAK2 or TNFRS1A expression display a severly blunted response to the tested cytokines.

2013-08-09 | GSE48848 | GEO

Detection of unbalanced insertions by aCGH and FISH

2011-02-28 | GSE27080 | GEO

MATT mapping of Transposon insertions sites of strain G27 GPS-cat library

2005-08-26 | GSE3197 | GEO

Oncogenic Enhancers from Small Genomic Insertions

Project description:The noncoding regions of tumor cell genomes harbor a considerable fraction of total variation, but the functional contribution of such variants to tumorigenesis is ill-defined. Among these noncoding variants, somatic insertions are among the least well-characterized due to challenges with interpreting short-read DNA sequences. To address this, we have identified enhancer-associated small insertion variants across a spectrum of tumor cells by using ChIP-seq to enrich and sequence enhancer DNA, and a computational approach with multiple alignment procedures to identify small insertions. Among the 82 tumor genomes studied here, small insertions were frequently observed in enhancer DNA sequences located near known oncogenes. Further study of one such insertion, found in primary leukemia tumor genomes, revealed that it nucleates formation of an active enhancer that drives expression of the LMO2 oncogene. The catalogue of enhancer-associated small insertion variants described here provides a foundation for further investigating the functions of this class of variants across a range of human cancers.

2016-07-08 | GSE76783 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data