Cryptic endogenous retrovirus subfamilies in the primate lineage
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1029531 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26419313_1.fastq.gz | Fastqsanger.gz | |||
| SRR26419313_2.fastq.gz | Fastqsanger.gz | |||
| SRR26419314_1.fastq.gz | Fastqsanger.gz | |||
| SRR26419314_2.fastq.gz | Fastqsanger.gz | |||
| SRR26419315_1.fastq.gz | Fastqsanger.gz |
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Project description:Many endogenous retroviruses (ERVs) in the human genome are primate-specific and contribute novel cis-regulatory elements and transcripts. Classification and annotation of ERVs, which are flanked by long terminal repeats (LTRs) containing sequences that control their transcriptional activity, is important to better understand their evolution and potential roles in the host. Here, we observed that many of the currently annotated LTR subfamilies spreading in the primate lineage have subsets of instances that appear to be misclassified. Focusing on the evolutionary young MER11A/B/C subfamilies, we performed a phylogenetic analysis and relied on cross-species conservation to reveal the presence of 4 phyletic groups, suggesting a new annotation for 412 (19.8%) of the MER11 instances. Next, we showed that the epigenetic heterogeneity observed within the MER11A/B/C subfamilies was better explained in the context of these new phyletic groups. Using a massively parallel reporter assay (MPRA), we also demonstrated the regulatory potential of the four phyletic groups and identified motifs that were associated with their differential activities. The MPRA combined with the use of phyletic groups across primates revealed an apes-specific gain of SOX related motifs through a single-nucleotide deletion. Finally, we applied a similar approach across all 53 simian-specific LTR subfamilies and determined the presence of 75 phyletic groups. We found that 3,807 (30.0%) instances from 26 of these LTR subfamilies changed annotation and could be characterized into one of these novel phyletic groups, many of which with a distinct epigenetic profile. This refined annotation of simian-specific LTRs could improve our understanding of the evolution of ERVs in primate genomes and reveal functional signals that would have been missed otherwise.
2023-10-23 | GSE245662 | GEO
Project description:BackgroundEndogenous retroviruses (ERVs), which blur the boundary between virus and transposable element, are genetic material derived from retroviruses and have important implications for evolution. This study examines the diversity and evolution of human endogenous retroviruses (HERVs) of the HERVL family, which has long terminal repeats (LTRs) named MLT2.ResultsBy probability-based sequence comparison, we uncover systematic annotation errors that conceal the true complexity and diversity of transposable elements (TEs) in the human genome. Our analysis identifies new subfamilies within the MLT2 group, proposes a refined classification scheme, and constructs new consensus sequences. We present an evolutionary analysis including phylogenetic trees that elucidate the relationships between these subfamilies and their contributions to human evolution. The results underscore the significance of accurate TE annotation in understanding genome evolution, highlighting the potential for misclassified TEs to impact interpretations of genomic studies.Availability and implementationNot applicable.
| S-EPMC11319637 | biostudies-literature
Project description:Germline piRNAs counteract endogenous retrovirus invasion from somatic cells
| PRJNA988107 | ENA
Project description:m6A methylation regulates the fate of endogenous retrovirus transcripts
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Project description:Background: Prion diseases such as bovine spongiform encephalopathies (BSE) are transmissible neurodegenerative diseases which are presumably caused by an infectious conformational isoform of the cellular prion protein. Previous work has provided evidence that in murine prion disease the endogenous retrovirus (ERV) expression is altered in the brain. To determine if prion-induced changes in ERV expression are a general phenomenon we used a non-human primate model for prion disease. Results: Cynomolgus macaques (Macaca fasicularis) were infected intracerebrally with BSE-positive brain stem material from cattle and allowed to develop prion disease. Brain tissue from the basis pontis and vermis cerebelli of the six animals and the same regions from four healthy controls were subjected to ERV expression profiling using a retrovirus-specific microarray and quantitative real-time PCR. We could show that Class I gammaretroviruses HERV-E4-1, ERV-9, and MacERV-4 increase expression in BSE-infected macaques. In a second approach, we analysed ERV-K-(HML-2) RNA and protein expression in extracts from the same cynomolgus macaques. Here we found a significant downregulation of both, the macaque ERV-K-(HML-2) Gag protein and RNA in the frontal/parietal cortex of BSE-infected macaques. Conclusions: We provide evidence that dysregulation of ERVs in response to BSE-infection can be detected on both, the RNA and the protein level. To our knowledge, this is the first report on the differential expression of ERV-derived structural proteins in prion disorders. Our findings suggest that endogenous retroviruses may induce or exacerbate the pathological consequences of prion-associated neurodegeneration. Cynomolgus macaques (Macaca fasicularis) were infected intracerebrally with BSE-positive brain stem material from cattle and allowed to develop prion disease. Brain tissue from the basis pontis and vermis cerebelli of the six animals and the same regions from four healthy controls were subjected to ERV expression profiling using a retrovirus-specific microarray and quantitative real-time PCR. In a second approach, ERV-K-(HML-2) RNA and protein expression was analysed in extracts from the same cynomolgus macaques.
2011-06-10 | E-GEOD-29818 | biostudies-arrayexpress
Project description:RNA sequencing of low-dose 5-azacytidine treated and PBS treated DLBCL cell lines to measure transcriptional changes in gene and endogenous retrovirus expression
2022-09-27 | GSE190319 | GEO
Project description:Background: Prion diseases such as bovine spongiform encephalopathies (BSE) are transmissible neurodegenerative diseases which are presumably caused by an infectious conformational isoform of the cellular prion protein. Previous work has provided evidence that in murine prion disease the endogenous retrovirus (ERV) expression is altered in the brain. To determine if prion-induced changes in ERV expression are a general phenomenon we used a non-human primate model for prion disease. Results: Cynomolgus macaques (Macaca fasicularis) were infected intracerebrally with BSE-positive brain stem material from cattle and allowed to develop prion disease. Brain tissue from the basis pontis and vermis cerebelli of the six animals and the same regions from four healthy controls were subjected to ERV expression profiling using a retrovirus-specific microarray and quantitative real-time PCR. We could show that Class I gammaretroviruses HERV-E4-1, ERV-9, and MacERV-4 increase expression in BSE-infected macaques. In a second approach, we analysed ERV-K-(HML-2) RNA and protein expression in extracts from the same cynomolgus macaques. Here we found a significant downregulation of both, the macaque ERV-K-(HML-2) Gag protein and RNA in the frontal/parietal cortex of BSE-infected macaques. Conclusions: We provide evidence that dysregulation of ERVs in response to BSE-infection can be detected on both, the RNA and the protein level. To our knowledge, this is the first report on the differential expression of ERV-derived structural proteins in prion disorders. Our findings suggest that endogenous retroviruses may induce or exacerbate the pathological consequences of prion-associated neurodegeneration.
2011-06-10 | GSE29818 | GEO
Project description:Speckled Protein 140 (SP140) is a chromatin reader with critical roles regulating immune cell transcriptional programs, and SP140 splice variants are associated with immune diseases including Crohn’s disease, multiple sclerosis, and chronic lymphocytic leukemia. SP140 expression is currently thought to be restricted to immune cells. However, by analyzing human transcriptomic datasets from a wide range of normal and cancer cell types, we found recurrent cancer-specific expression of SP140, driven by an alternative intronic promoter derived from an intronic endogenous retrovirus (ERV). The ERV belongs to the primate-specific LTR8B family. The ERV drives expression of multiple cancer-specific isoforms, including a nearly full-length isoform that retains all the functional domains of the full-length canonical isoform and is also localized within the nucleus, consistent with a role in chromatin regulation. In a fibrosarcoma cell line, silencing the cancer-specific ERV promoter of SP140 resulted in increased sensitivity to interferon-mediated cytotoxicity and dysregulation of multiple genes. Our findings implicate aberrant ERV-mediated SP140 expression as a novel mechanism contributing to immune gene dysregulation in a wide range of cancer cells.
2024-02-20 | GSE256003 | GEO
Project description:Speckled Protein 140 (SP140) is a chromatin reader with critical roles regulating immune cell transcriptional programs, and SP140 splice variants are associated with immune diseases including Crohn’s disease, multiple sclerosis, and chronic lymphocytic leukemia. SP140 expression is currently thought to be restricted to immune cells. However, by analyzing human transcriptomic datasets from a wide range of normal and cancer cell types, we found recurrent cancer-specific expression of SP140, driven by an alternative intronic promoter derived from an intronic endogenous retrovirus (ERV). The ERV belongs to the primate-specific LTR8B family. The ERV drives expression of multiple cancer-specific isoforms, including a nearly full-length isoform that retains all the functional domains of the full-length canonical isoform and is also localized within the nucleus, consistent with a role in chromatin regulation. In a fibrosarcoma cell line, silencing the cancer-specific ERV promoter of SP140 resulted in increased sensitivity to interferon-mediated cytotoxicity and dysregulation of multiple genes. Our findings implicate aberrant ERV-mediated SP140 expression as a novel mechanism contributing to immune gene dysregulation in a wide range of cancer cells.
2024-02-20 | GSE256010 | GEO
Project description:m6A methylation regulates the fate of endogenous retrovirus transcripts [CUT & RUN]
| PRJNA656303 | ENA