Ontology highlight
ABSTRACT:
PROVIDER: PRJEB11973 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1157300_1.fastq.gz | Fastqsanger.gz | |||
| ERR1157300_2.fastq.gz | Fastqsanger.gz | |||
| ERR1157310_1.fastq.gz | Fastqsanger.gz | |||
| ERR1157310_2.fastq.gz | Fastqsanger.gz | |||
| ERR1157320_1.fastq.gz | Fastqsanger.gz |
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Project description:We used ATLAS-seq-neo to map the sites of integration of an engineered LINE-1 (L1) retrotransposon into the genome of HeLa S3 cells. In brief, we transfected cells with a plasmid-borne L1.3 element carrying a neomycin-resistance-based retrotransposition cassette, as well as a hygromycin-resistance cassette on the plasmid backbone. For this set of experiments, cells were only selected for transfection (hygromycin) but not for retrotransposition (neomycin). Then we prepared ATLAS-seq-neo libraries. Each sample corresponds to an independent transfection and pool of hygromycin-resistant cells. ATLAS-seq-neo relies on the random mechanical fragmentation of the genomic DNA to ensure high-coverage, ligation of adapter sequences, suppression PCR-amplification of the 3' end L1 junction with its flanking genomic sequence, and Ion Torrent sequencing using single-end 400 bp read chemistry. The primer used for suppression PCR specifically targets the engineered element and not endogenous copies as in the original ATLAS-seq protocol (Philippe et al. eLife 2016). For some libraries, the linker-ligated genomic DNA was digested with BamHI, which cuts downstream of L1 polyA site in the plasmid backbone, to limit amplification from the plasmid and enrich for retrotransposition-mediated insertion events into the genomic DNA.
2019-04-03 | E-MTAB-7644 | biostudies-arrayexpress
Project description:Host proteins regulate LINE-1 (L1) retrotransposition. Here, we use immunoprecipitation followed by liquid chromatography-tandem mass spectrometry to identify proteins that associate with the L1 ORF1-encoded protein (ORF1p) in ribonucleoprotein particles.
2023-03-11 | PXD038851 | Pride
Project description:We report that TAR DNA binding protein 43 (TDP-43), mutations in which constitute a major risk factor for amyotrophic lateral sclerosis (ALS), inhibits L1 retrotransposition in mouse embryonic stem cells (mESCs) and preimplantation embryos. Knockdown of TDP-43 resulted in massive genomic L1 expansion and impaired cell growth in preimplantation embryos and ESCs. Functional analysis demonstrated that TDP-43 interacts with L1 open reading frame 1 protein (L1 ORF1p) to mediate genomic protection, and loss of this interaction led to de-repression of L1 retrotransposition. Our results identify TDP-43 as a guardian of the embryonic genome by protecting it from massive L1 retrotransposition.
2023-01-04 | GSE199197 | GEO
Project description:L1 retrotransposons are active elements in the genome, capable of mobilization in neuronal progenitor cells. Previously, we showed that chromatin remodeling during neuronal differentiation allows for a transient stimulation of L1 transcription. The activity of L1 retrotransposons during brain development can impact gene expression and neuronal function. Here we show that L1 neuronal retrotransposition in rodents is increased in the absence of MeCP2, a protein involved in global methylation and human neurodevelopmental diseases. Using neuronal progenitor cells derived from human induced pluripotent stem cells and human tissues, we revealed that Rett syndrome patients, with MeCP2 mutations, have increased susceptibility for L1 retrotransposition. Our data demonstrate that disease-related genetic mutations can influence the frequency of neuronal L1 retrotransposition, thereby increasing brain-specific genetic mosaicism.
2010-11-11 | GSE21037 | GEO
Project description:L1 retrotransposons are active elements in the genome, capable of mobilization in neuronal progenitor cells. Previously, we showed that chromatin remodeling during neuronal differentiation allows for a transient stimulation of L1 transcription. The activity of L1 retrotransposons during brain development can impact gene expression and neuronal function. Here we show that L1 neuronal retrotransposition in rodents is increased in the absence of MeCP2, a protein involved in global methylation and human neurodevelopmental diseases. Using neuronal progenitor cells derived from human induced pluripotent stem cells and human tissues, we revealed that Rett syndrome patients, with MeCP2 mutations, have increased susceptibility for L1 retrotransposition. Our data demonstrate that disease-related genetic mutations can influence the frequency of neuronal L1 retrotransposition, thereby increasing brain-specific genetic mosaicism. Genetic reprogramming of somatic cells to a pluripotent state (induced pluripotent stem cells, or iPSCs) by over-expression of specific genes has been accomplished for fibroblasts derived from controls and Rett syndrome patients. Different clones from each were compared to respective original fibroblasts and a human embryonic stem cell line. Gene expression profiles measured using human genome Affymetrix Gene Chip arrays were grouped by hierarchical clustering, and correlation coefficients were computed for all pair-wise comparisons.
2010-11-11 | E-GEOD-21037 | biostudies-arrayexpress
Project description:Transposable elements (TEs) are now recognized not only as parasitic DNA, whose spread in the genome must be controlled by the host, but also as major players in shaping genome evolution and providing genetic substrates for evolving new regulatory functions. Long INterspersed Element-1 (LINE-1 or L1), the only currently autonomous mobile transposon in humans, occupies 17% of the genome and continues to generate inter- and intra-individual genetic variation, in some cases resulting in disease. Nonetheless, our knowledge of how L1 activity is controlled and what function L1s play in host gene regulation remains fragmentary. Here, we use CRISPR/Cas9 screening strategies in two distinct human cell lines to provide the first genome-wide survey of genes involved in L1 retrotransposition control. Through this approach we identified functionally diverse genes that either promote or restrict L1 retrotransposition. These factors control the L1 life cycle at transcriptional or post-transcriptional levels, and in a manner which in some, but not in other cases depends on the endogenous L1 sequence, underscoring the complexity of L1 regulation. We further investigated L1 restriction by three candidate regulators, MORC2 and HUSH (human silencing hub) complex subunits TASOR and MPP8. HUSH/MORC2 selectively bind evolutionarily young, full-length L1s immersed within transcriptionally permissive euchromatic environment, and promote H3K9me3 deposition for transcriptional silencing. Interestingly, these silencing events often occur within introns of transcriptionally active host genes, and lead to down-regulation of host gene expression in a HUSH/MORC2-dependent manner. Together, our data provide a rich resource for studies of L1 retrotransposition, elucidate a novel L1 restriction pathway, and illustrate how epigenetic silencing of TEs can influence host gene expression programs.
2017-12-06 | GSE95374 | GEO
Project description:Long interspersed elements 1 (LINE-1 or L1) are retrotransposons that dominate the mouse genomic landscape, and are expressed in Embryonic Stem Cells (ESCs), germ cells, and during early development. Based on clear precedents in plants and fission yeast, we investigated in this study a role for RNAi and other RNA degradation pathways in the regulation of L1 expression and mobilization. We uncovered the existence of novel small (s)RNAs that map to active L1 elements. Some of these sRNAs have characteristics of cognate short-interfering RNA populations, while others display length heterogeneity that evokes a biogenesis through a RNA surveillance pathway, in a Dicer-independent manner. We additionally found that genetic ablation of Dicer and the sRNA effector protein AGO2 has complex and profound consequences on L1 transcription and mobilization in ESCs, indicating that endogenous RNA interference (RNAi) pathway indeed maintain genomic integrity against L1 proliferation. Finally, we investigated the implication of L1 retrotransposition during ESC differentiation and propose that the mobilization of L1 elements in Dicer mutant ESCs could partially explain the inability of these cells to differentiate. 2 samples examined: WT E14 and Dicer mutant mouse ESCs
2013-12-11 | E-GEOD-43110 | biostudies-arrayexpress
Project description:Somatic retrotranspositions of various mobile genetic elements take place in tumors, and L1 retroelements physiologically transpose in neural progenitor cells during neurogenesis. We sequenced whole genomes of the neural progenitor cell-derived subependymal giant cell astrocytomas that typically affect patients suffering from the neurodevelopmental disease Tuberous Sclerosis. Here we show an unprecedented increased L1 retrotransposition in these tumors, with tens of thousands new genomic insertions, that preferentially invade genes involved in neural activity, synaptic transmission and cancer. The prevalent insertions are short, nested in preexisting L1 repeats in the same orientation, trimmed in both the 5’ and 3’ ends, representing unorthodox retrotransposition”. Most somatic L1 inserts in the genomically stable astrocytomas are nested in preexisting L1 elements. This preferred nested integration may act as a “lightning rod” mechanism dampening the effects of massive retrotransposition. In contrast, the enhanced transposition found in genomically unstable breast tumors includes regions of high-density clustered insertion, transposminos. These clustered insertions are expected to be more detrimental, as many of them are non-nested and frequently invade genic and exonic sequences. Exaggerated L1 retrotransposition may be a common stochastic damaging pathway in neurological disorders and cancer.
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