Similar Datasets
Project description:We found that the germline transcription factor double homeobox 4 (DUX4) is upregulated upon infection with wild-type herpes simplex virus-1 (HSV-1). The goal of this experiment was to compare the cellular transcriptome of HEK293T cells that were infected with HSV-1 (KOS strain), or transfected with a plasmid encoding human DUX4.
2018-09-19 | GSE101435 | GEO
Project description:RNAseq analysis of THP-1 cells mock-infected or infected with HSV-1 without or with DUX4 knockdown
2024-11-24 | GSE279339 | GEO
Project description:Chromatin immunoprecipitation sequencing of transcription factor DUX4
| PRJNA1201583 | ENA
Project description:DUX4 is generally agreed to underlie pathology in Facioscapulohumeral muscular dystrophy Microarrays were used to examine gene expression after primary murine satellite cell-derived myoblasts were retrovirally infected with constructs encoding DUX4, DUX4c, constitutively active, dominant negative and truncated DUX4 versions.
2017-01-31 | GSE77100 | GEO
Project description:Double homeobox 4 (DUX4) is expressed in at the early preimplantation stage in human embryos. Here we show that induced human DUX4 expression substantially alters the non-coding chromatin accessibility of non-coding DNA and activates thousands of newly identified putative transcribed enhancer-like regions, preferentially located within ERVL-MaLR repeat elements. CRISPR activation of transcribed enhancers by C-terminal DUX4 motifs results in the increased expression of target embryonic genome activation (EGA) genes ZSCAN4 and KHDC1P1. We show that DUX4 is markedly enriched in human zygotes, followed by intense nuclear DUX4 localization preceding and coinciding with minor EGA. DUX4 knockdown in human zygotes led to changes in the EGA transcriptome but did not terminate the embryos. We also show that the DUX4 protein interacts with the Mediator complex via the C-terminal KIX binding motif. Our findings contribute to the understanding of DUX4 as a regulator of the non-coding genome.
2022-03-16 | GSE171803 | GEO
Project description:We describe the role of the cellular transcription factor DUX4 in the regulation of herpesviral gene expression.
2021-05-21 | GSE174759 | GEO
Project description:Single cell RNA sequencing was performed on a CML derived cell line, which contains a TET-ON inducible system for DUX4 inducible expression (DIE). In attempt of finding key players early in the DUX4 induced process, we performed single-cell RNA sequencing (SCS) on induced DIE cells, as early as 2 hours after induction. In a sequential manner, DIE cells induced for 3, 4, and 6 hours were also collected and used for SCS. By analysing these cells at a single cell level, we aimed to find (subtle) changes in the DIE cell transcriptome, that start early after DUX4 induction.
2021-01-01 | GSE156154 | GEO
Project description:Bulk RNA sequencing was performed on a CML derived cell line, which contains an TET-ON inducible system for DUX4 inducible expression (DIE). Due to the unconventional cellular background used for the generation of an inducible FSHD cell line, bulk RNA seq was performed to determine if, and otherwise to what extend, this cellular background inteferes with the transcriptional program DUX4 is known to activate in muscle cells.
2020-07-29 | GSE154649 | GEO
Project description:The aim of this study is to define the molecular mechanisms underlying DUX4-associated toxicity in the context of facioscapulohumeral muscular dystrophy (FSHD). DUX4 is a transcription factor, which induces cell death by activating the transcription of its targets. No molecule able to directly control DUX4 activity is currently known. By using a tandem affinity purification protocol combined to mass spectrometry analysis, we identified Matrin 3 (MATR3), as the first cellular factor able to directly block DUX4 toxic activity. We found that MATR3 binds to the DNA binding domain of DUX4 blocking the activation of its genomic targets.
2023-08-21 | PXD011073 | Pride
Project description:DUX4 is a double homeodomain transcription factor whose misexpression in the muscle causes facioscapulohumeral muscular dystrophy (FSHD). The transcriptional activity of DUX4 has been extensively characterized, and is thought to be the primary driver of FSHD pathogenesis. Yet, DUX4 expression lowers the protein level of an RNA quality control factor, UPF1, without affecting its transcript level, hinting at post-transcriptional regulatory activity downstream of DUX4 expression. How extensive the post-transcriptional activity of DUX4 is, and how relevant it is to FSHD pathogenesis, is unknown. In order to gain insight into DUX4-induced post-transcriptional gene regulation, we measured transcript and protein levels in DUX4 expressing cells via RNA-seq and SILAC-based quantitative mass spectrometry, respectively. We show that DUX4 transcriptional targets are robustly translated, including those genes previously identified as potential FSHD biomarkers. However, comparing the overall pattern of gene expression changes for RNA versus protein reveals striking differences in the most highly activated pathways, with the former showing changes in RNA processing and splicing, and the latter affecting the humoral immune response, proteolysis and exocytosis, among other pathways. Consistent with a misregulation of exocytosis, fluorescence imaging shows fragmented golgi apparatus in DUX4-expressing cells. Of the genes that showed discordant RNA and protein expression levels, post-transcriptional buffering was particularly evident for genes involved in stress response and may explain why DUX4-expressing cells succumb to toxicity despite robust transcriptional activation of stress response genes. Moreover, several genes involved in RNA decay including UPF1, UPF3B, SMG6 and XRN1 showed downregulation at the protein level, which may explain the massive inhibition of RNA quality control in DUX4-expressing cells. These results highlight the importance of considering post-transcriptional gene regulation in DUX4-expressing cells in order to fully understand the FSHD disease process.
2019-01-21 | PXD010221 | Pride