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Altered TE-derived genes leads to pathogenesis of FXD [PacBioRNASeq]

ABSTRACT: We identified known and unknown transposon elements in the cells from healthy donors, FXD patients, and ALL patients by long-read RNA-sequencing. Using these identified TEs, we analyzed the expression of TE-derived genes by shot-read (illumina) RNA-sequencing. We found that expression of some specific TE-derived genes were changed in FXD compared to those in healthy donors. These findings suggested the involvement of modified expressions of TE-derived genes in the pathogenesis of FXD.

ORGANISM(S): Homo sapiens

PROVIDER: GSE264089 | GEO | 2024/10/30

REPOSITORIES: GEO

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Altered TE-derived genes leads to pathogenesis of FXD [ShortReadRNASeq]

Project description:We identified known and unknown transposon elements in the cells from healthy donors, FXD patients, and ALL patients by long-read RNA-sequencing. Using these identified TEs, we analyzed the expression of TE-derived genes by shot-read (illumina) RNA-sequencing. We found that expression of some specific TE-derived genes were changed in FXD compared to those in healthy donors. These findings suggested the involvement of modified expressions of TE-derived genes in the pathogenesis of FXD.

2024-10-30 | GSE264090 | GEO

LocusMasterTE: long-read assisted short-read TE quantification [short]

Project description:With an ability to compromise genome integrity, transposable elements (TEs) have significant associations with human diseases. Short-read sequencing has been used to study the expression of TEs; however, the highly repetitive nature of these elements makes multimapping a critical issue. Here we implement LocusMasterTE, an improved quantification method by integrating long-read sequencing. Introducing computed transcript per million(TPM) counts from long-read sequencing as prior distribution during Expectation-Maximization(EM) model in short-read TE quantification, multi-mapped reads are re-assigned to correct expression values. Based on simulated short reads, LocusMasterTE outperforms current quantitative approaches and is significantly favorable in capturing newly inserted TEs. We also verified that TEs quantified by LocusMasterTE clearly related to euchromatins and heterochromatins in cell line samples. With LocusMasterTE we anticipate that more accurate quantification can be performed, allowing novel functions of TEs to be uncovered.

2023-09-01 | GSE225380 | GEO

Altered TE-derived genes leads to pathogenesis of FXD

Project description:Altered TE-derived genes leads to pathogenesis of FXD

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LocusMasterTE: long-read assisted short-read RNA-seq TE quantification [long]

2023-09-01 | GSE225377 | GEO

TE-Seq: A Transposable Element Annotation and RNA-Seq Pipeline

Project description:The TE-Seq pipeline conducts an end-to-end analysis of RNA sequencing data, examining both genes and TEs. It implements the most current computational methods tailor-made for TEs, and produces a comprehensive analysis of TE expression at both the level of the individual element and at the TE clade level. Furthermore, if supplied with long-read DNA sequencing data, it is able to assess TE expression from non-reference (polymorphic) loci. As a demonstration, we analyzed proliferating, early senescent, and late senescent lung fibroblast RNA-Seq data, and created a custom reference genome and annotations for this cell strain using Nanopore sequencing data. We found that several retrotransposable element (RTE) clades were upregulated in senescence, which included non-reference, intact, and potentially active elements.

2024-11-10 | GSE280365 | GEO

Altered TE-derived genes leads to pathogenesis of FXD [PacBioRNASeq]

Project description:Altered TE-derived genes leads to pathogenesis of FXD [PacBioRNASeq]

| PRJNA1100964 | ENA

Altered TE-derived genes leads to pathogenesis of FXD [ShortReadRNASeq]

Project description:Altered TE-derived genes leads to pathogenesis of FXD [ShortReadRNASeq]

| PRJNA1100965 | ENA

TE-associated chromatin variation in mice livers

Project description:Chromatin accessibility is a hallmark of active regulatory function in the genome and variation of chromatin accessibility across individuals has been shown to contribute to complex traits and disease susceptibility. However, the mechanisms responsible for chromatin variation among different individuals and how this variation contributes to phenotypic diversity remain poorly understood. We examined chromatin accessibility variation in liver tissue from seven strains of adult mice that have phenotypic diversity in response to a high-fat/high-sucrose diet. Remarkably, nearly 40% of the loci with the greatest degree of chromatin variability across the strains are associated with transposable elements (TEs), with evolutionarily younger TEs being particularly enriched for regions of chromatin variation. We found that evolutionary younger and older TEs have differential chromatin accessibility profiles and are enriched for binding sites of different transcription factors, indicating the role of TEs in the evolution of regulatory networks in the liver. We also demonstrate that TE polymorphisms and epigenetic regulation of TEs contribute to regulatory variation across different strains through providing binding sites for liver transcription factors. Intriguingly, variable chromatin loci that are associated with liver metabolism are primarily TE-associated. We demonstrate that TEs contribute to regulatory variation in liver and have downstream effects on metabolism. Our data reveal TEs as a novel and important contributor to regulatory and phenotypic variation in the liver and suggest that regulatory variation at TEs is a major contributor to phenotypic variation in populations. Examination of chromatin accessibility with FAIRE-seq in livers of male mice (A/J, AKR/J, BALB/cJ, C57BL/6J, C3H/HeJ, CBA/J, DBA/2J, BXH2/TyJ, and BXH19/TyJ) fed a high-fat, high-sucrose diet.

2016-07-14 | E-GEOD-75770 | biostudies-arrayexpress

Using long-read CAGE sequencing to profile cryptic-promoter derived transcripts and their contribution to the immunopeptidome

Project description:Recent studies have demonstrated that the non-coding genome can produce unannotated proteins as antigens that induce immune response. One major source of this activity is the aberrant epigenetic reactivation of transposable elements (TEs). In tumors, TEs often provide cryptic or alternate promoters, which can generate transcripts that encode tumor-specific unannotated proteins. Thus, TE-derived transcripts have the potential to produce tumor-specific, but recurrent, antigens shared among many tumors. Identification of TE-derived tumor antigens holds the promise to improve cancer immunotherapy approaches; however, current genomics and computational tools are not optimized for their detection. Here we combined CAGE technology with full-length long-read transcriptome sequencing (Long-Read CAGE, or LRCAGE) and developed a suite of computational tools to significantly improve immunopeptidome detection by incorporating TE-derived and other tumor transcripts into the proteome database. By applying our methods to human lung cancer cell line H1299 data, we demonstrated that long-read technology significantly improves mapping of promoters with low mappability scores and LRCAGE guarantees accurate construction of uncharacterized 5’ transcript structure. Unannotated peptides predicted from newly characterized transcripts were readily detectable in whole cell lysate mass-spectrometry data. Incorporating unannotated peptides into the proteome database enabled us to detect non-canonical antigens in HLA-pulldown LC-MS/MS data. At last, we showed that epigenetic treatment increased the number of non-canonical antigens, particularly those encoded by TE-derived transcripts, which might expand the pool of targetable antigens for cancers with low mutational burden.

2023-09-23 | PXD040265 | Pride

Transposable element targeting by piRNAs in Laurasiatherians with distinct TE activities

Project description:Transposable elements (TEs) are self-mobilizing elements that make up a large fraction of mammalian genomes. PIWI proteins and PIWI interacting RNAs (piRNAs) are a part of a system aimed at controlling and preventing TE proliferation. We examined the TE landscape and piRNA repertoires from three non-model Laurasiatherian mammals (dog, horse and big brown bat) with differing TE complements and proliferation patterns to address questions about the evolutionary relationships between piRNAs and TEs. We found that the genomic abundance of new TEs may not match TE transcription. We speculate that a higher rate of SINE targeting by piRNAs in the horse genome contributed to the reduced SINE insertion rate.

2017-03-26 | GSE56336 | GEO

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