Ontology highlight
ABSTRACT:
PROVIDER: PRJNA643792 | ENA |
REPOSITORIES: ENA
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Project description:Transposable elements (TEs) sequence capture
| PRJEB11704 | ENA
Project description:Background: Transposable elements are known to influence the regulation of some genes. We aimed to determine which genes show altered gene expression when transposable elements are epigenetically activated. Results: We find over 2000 genes with altered steady-state expression levels in ddm1 mutants. Some of these genes are influenced by neighboring transposable element fragments, while other genes are targeted by transposable element derived 21 nucleotide siRNAs. Conclusion: The regulation of the genic portion of the Arabidopsis genome is heavily influenced by the epigenetic regulation of transposable elements. The regulation of genes by transposable elements can occur through multiple mechanisms. Three biological replicates for two genotypes
2014-04-07 | E-GEOD-46050 | biostudies-arrayexpress
Project description:Virophages are small dsDNA viruses dependent on a nucleocytoplasmic large-DNA virus infection of a cellular host for replication. Putative virophages infecting algal hosts are classified together with Polinton-like viruses, transposable elements widely found in algal genomes, yet the lack of isolated strains raises questions about their existence as independent entities. We isolated and characterized a virophage (PgVV-14T) co-infecting Phaeocystis globosa with the Phaeocystis globosa virus-14T (PgV-14T).
2023-02-11 | PXD036892 | Pride
Project description:Host macrophage transcriptional responses to intracellular pathogens remain poorly characterized. We screened transcriptional enhancers engaged in response to M. tuberculosis (Mtb) infection by ChIPseq analysis of histone H3 lysine 4 monomethylation (H3K4me1). De novo monomethylation during infection was associated with genes implicated in host defense and apoptosis. These regions were enriched for binding sites for ETS transcription factor family members and response elements for nuclear receptors, including liver X receptors (LXRs) and peroxisomal proliferator activated receptors (PPARs), many of which were encompassed by transposable elements. LXRa expression was strongly induced by infection, whereas that of PPARs was unaffected. LXR DNA binding and NCoR corepressor recruitment increased proportionately in infected cells but coactivator association was unchanged, consistent with a lack of induction of endogenous agonists. However, treatment of infected cells with LXR agonist T0901317 strongly increased coactivator recruitment and induced a gene expression program characterized by enhanced innate immune signaling and lipid metabolism. Remarkably, T0901317 treatment selectively induced apoptosis in infected macrophages, and was accompanied by Mtb death, reducing mycobacterial burden 18-fold relative to vehicle 5d after infection. These studies define macrophage transcriptional responses to Mtb infection, and suggest that tissue-specific LXRa agonists may be efficacious in clinical management of tuberculosis.
2015-10-15 | E-MTAB-3192 | biostudies-arrayexpress
Project description:Transposable elements hold regulatory functions to impact cell fate determination by controlling gene expression, which when altered can promote oncogenesis. Despite accounting for half of the human genome, little is known about the transcriptional mechanisms that confer regulatory properties to transposable elements in pluripotent, mature versus oncogenic cell states. Through positional analysis over repetitive DNA sequence of H3K27ac ChIP-seq from 32 different normal cell and tissue states, we report pluripotent stem and mature cell states-specific “regulatory transposable elements”. Those specific to pluripotent stem cells are binding sites for the pluripotency factors NANOG, SOX2 and OCT4. In mature cell and tissue states, regulatory transposable elements are docking sites for lineage-specific transcription factors, such as AR and FOXA1 in benign prostate epithelium. Expanding the positional analysis to localized prostate tumors, we show how cancer cell states remaining dependent on AR share regulatory transposable elements with pluripotent stem cells. These include regulatory transposable elements, such as Tigger3a, that serve as binding sites for AR and whose regulatory functions are required for prostate cancer cell growth. Together, our results suggest that oncogenesis differs from normal cell fate determination by hijacking pluripotent stem cells regulatory transposable elements that serve as docking sites for lineage-specific transcription factors.
2023-09-08 | GSE224687 | GEO
Project description:Endogenous retroviruses (ERVs) are transposable elements that cause host genome instability and usually play deleterious roles such as tumorigenesis. Recent advances also suggest that this 'enemy within' may encode viral mimic to induce antiviral immune responses through viral sensors. Here, through whole genome RNA-seq we discovered a full-length ERV-derived long non-coding RNA (lncRNA), designated lnc-EPAV (ERV-derived lncRNA positively regulates antiviral responses), as a positive regulator of NF-κB signaling. Lnc-EPAV expression was rapidly up-regulated by viral RNA mimic or RNA viruses to facilitate the expression of RELA, an NF-κB subunit that plays a critical role in antiviral responses. In turn, RELA promoted the transcription of lnc-EPAV to form a positive feedback loop. Transcriptome analysis of lnc-EPAV-silenced macrophages, combined with gain- and loss-of-function experiments, showed that lnc-EPAV was critical for induction of type I interferon (IFN) and inflammatory cytokine expression by RNA viruses. Consistently, lnc-EPAV-deficient mice exhibited reduced expression of type I IFNs, and consequently increased viral loads and mortality following lethal RNA virus infection. Mechanistically, lnc-EPAV promoted expression of RELA by competitively binding to and displacing SFPQ, a transcriptional repressor of RELA. The binding between ERV-derived RNAs and SFPQ also existed in human cells. Altogether, our work demonstrates an alternative mechanism by which ERVs regulate antiviral immune responses.
2018-11-07 | PXD011577 | Pride