Epigenetic control of genes and transposable elements [Knockdown RNA-seq]
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE108087 | GEO | 2018/12/11
REPOSITORIES: GEO
Similar Datasets
Project description:Epigenetic control is an elaborate system the cell uses to control aspects of cell type and gene control. Histones and DNA are chemically modified to signal epigenetic information as to whether a gene is active or inactive, and so maintain cell type stability. Whilst epigenetic control of genes has been explored, the control of the rest of the genome is less well explored. The bulk of DNA and chromatin consists of repetitive elements, not genes, and these TEs must be tightly regulated to provide structure and function for nearby genes and, ultimately, cell type control. In this project we explore the intereaction of epigenetic control factors, and inhibitors, and how perturbation of the epigenetic control system disrupts TE regulation inside embryonic stem cells.
2018-12-11 | GSE108086 | GEO
Project description:Epigenetic control is an elaborate system the cell uses to control aspects of cell type and gene control. Histones and DNA are chemically modified to signal epigenetic information as to whether a gene is active or inactive, and so maintain cell type stability. Whilst epigenetic control of genes has been explored, the control of the rest of the genome is less well explored. The bulk of DNA and chromatin consists of repetitive elements, not genes, and these TEs must be tightly regulated to provide structure and function for nearby genes and, ultimately, cell type control. In this project we explore the intereaction of epigenetic control factors, and inhibitors, and how perturbation of the epigenetic control system disrupts TE regulation inside embryonic stem cells.
2018-12-11 | GSE108090 | GEO
Project description:Investigation of the effect of the knockdown of AT-hook motif DNA binding nuclear matrix protein TRANSPOSABLE ELEMENT KILLER (TEK) in the Arabidopsis Landsberg erecta (Ler) background Transposable elements (TEs) are silenced by epigenetic mechanisms of DNA and histone methylation. The repressive histone modification H3 lysine 9 dimethylation (H3K9me2) is TE-associated epigenetic hallmark, and is necessary for DNA methylation. However the mechanism to direct the repressive epigenetic modification in TEs has remained elusive. Here we show that knockdown of the AT-hook motif DNA binding nuclear matrix protein TRANSPOSABLE ELEMENT KILLER (TEK) in the Arabidopsis Landsberg erecta (Ler) background results in robust activation of various TEs, the repeat-containing floral repressor gene FWA and the TE-containing floral repressor FLOWERING LOCUS C (FLC). A four chip study using two separate wild-type seedling mRNA samples and two separate TEKi seedling mRNA samples
2012-09-12 | E-GEOD-39158 | biostudies-arrayexpress
Project description:The hematopoietic system relies on the dynamic control of transcriptional regulatory networks, yet our understanding of the mechanisms that dictate the generation of diverse, mature progeny from hematopoietic stem cells are continuously evolving. Transposable elements (TEs) in the human genome and their chromatin regulators are implicated to sculpt the regulatory networks of immune cells. We systematically dissected the contributions of TEs to human hematopoiesis and demonstrated that TEs play instructive roles in lineage determination from primary human hematopoietic stem and progenitor cells. We built a comprehensive, cell type resolved enhancer-gene atlas of the human hematopoietic system and identified that TEs contribute to cell type and lineage specific enhancers. TEs exhibited dynamic transcription during lymphoid differentiation. Chemical and genetic perturbation of regulators of heterochromatin within primary human hematopoietic stem and progenitor cells derepressed TEs and elicited lineage biases during lymphoid differentiation. Knockout of the H3K9 methyltransferase EHMT1 or the heterochromatin adaptor protein TRIM28 resulted in lineage skewing to natural killer (NK) cells at the expense of B and T cells. Single cell RNA and ATAC-sequencing revealed that lineage skewing manifested early within hematopoietic progenitors. Further, knockout of TRIM28 or EHMT1 generated NK cells with distinct effector functions, where loss of TRIM28 resulted in enhanced IFN-ɣ producing NK cells and loss of EHMT1 enhanced the generation of CD16+ NK cells. Distinct TE families were epigenetically derepressed in EHMT1 versus TRIM28 knockout NK cells, yet enriched for NK-relevant transcription factor motifs. Modulation of heterochromatin machinery underscores the role of TEs in human hematopoietic differentiation and enables novel approaches to derive diverse NK cell subtypes for adoptive cell therapies.
2024-05-31 | GSE232104 | GEO
Project description:The hematopoietic system relies on the dynamic control of transcriptional regulatory networks, yet our understanding of the mechanisms that dictate the generation of diverse, mature progeny from hematopoietic stem cells are continuously evolving. Transposable elements (TEs) in the human genome and their chromatin regulators are implicated to sculpt the regulatory networks of immune cells. We systematically dissected the contributions of TEs to human hematopoiesis and demonstrated that TEs play instructive roles in lineage determination from primary human hematopoietic stem and progenitor cells. We built a comprehensive, cell type resolved enhancer-gene atlas of the human hematopoietic system and identified that TEs contribute to cell type and lineage specific enhancers. TEs exhibited dynamic transcription during lymphoid differentiation. Chemical and genetic perturbation of regulators of heterochromatin within primary human hematopoietic stem and progenitor cells derepressed TEs and elicited lineage biases during lymphoid differentiation. Knockout of the H3K9 methyltransferase EHMT1 or the heterochromatin adaptor protein TRIM28 resulted in lineage skewing to natural killer (NK) cells at the expense of B and T cells. Single cell RNA and ATAC-sequencing revealed that lineage skewing manifested early within hematopoietic progenitors. Further, knockout of TRIM28 or EHMT1 generated NK cells with distinct effector functions, where loss of TRIM28 resulted in enhanced IFN-ɣ producing NK cells and loss of EHMT1 enhanced the generation of CD16+ NK cells. Distinct TE families were epigenetically derepressed in EHMT1 versus TRIM28 knockout NK cells, yet enriched for NK-relevant transcription factor motifs. Modulation of heterochromatin machinery underscores the role of TEs in human hematopoietic differentiation and enables novel approaches to derive diverse NK cell subtypes for adoptive cell therapies.
2024-05-31 | GSE232103 | GEO
Project description:The hematopoietic system relies on the dynamic control of transcriptional regulatory networks, yet our understanding of the mechanisms that dictate the generation of diverse, mature progeny from hematopoietic stem cells are continuously evolving. Transposable elements (TEs) in the human genome and their chromatin regulators are implicated to sculpt the regulatory networks of immune cells. We systematically dissected the contributions of TEs to human hematopoiesis and demonstrated that TEs play instructive roles in lineage determination from primary human hematopoietic stem and progenitor cells. We built a comprehensive, cell type resolved enhancer-gene atlas of the human hematopoietic system and identified that TEs contribute to cell type and lineage specific enhancers. TEs exhibited dynamic transcription during lymphoid differentiation. Chemical and genetic perturbation of regulators of heterochromatin within primary human hematopoietic stem and progenitor cells derepressed TEs and elicited lineage biases during lymphoid differentiation. Knockout of the H3K9 methyltransferase EHMT1 or the heterochromatin adaptor protein TRIM28 resulted in lineage skewing to natural killer (NK) cells at the expense of B and T cells. Single cell RNA and ATAC-sequencing revealed that lineage skewing manifested early within hematopoietic progenitors. Further, knockout of TRIM28 or EHMT1 generated NK cells with distinct effector functions, where loss of TRIM28 resulted in enhanced IFN-ɣ producing NK cells and loss of EHMT1 enhanced the generation of CD16+ NK cells. Distinct TE families were epigenetically derepressed in EHMT1 versus TRIM28 knockout NK cells, yet enriched for NK-relevant transcription factor motifs. Modulation of heterochromatin machinery underscores the role of TEs in human hematopoietic differentiation and enables novel approaches to derive diverse NK cell subtypes for adoptive cell therapies.
2024-05-31 | GSE232102 | GEO
Project description:The hematopoietic system relies on the dynamic control of transcriptional regulatory networks, yet our understanding of the mechanisms that dictate the generation of diverse, mature progeny from hematopoietic stem cells are continuously evolving. Transposable elements (TEs) in the human genome and their chromatin regulators are implicated to sculpt the regulatory networks of immune cells. We systematically dissected the contributions of TEs to human hematopoiesis and demonstrated that TEs play instructive roles in lineage determination from primary human hematopoietic stem and progenitor cells. We built a comprehensive, cell type resolved enhancer-gene atlas of the human hematopoietic system and identified that TEs contribute to cell type and lineage specific enhancers. TEs exhibited dynamic transcription during lymphoid differentiation. Chemical and genetic perturbation of regulators of heterochromatin within primary human hematopoietic stem and progenitor cells derepressed TEs and elicited lineage biases during lymphoid differentiation. Knockout of the H3K9 methyltransferase EHMT1 or the heterochromatin adaptor protein TRIM28 resulted in lineage skewing to natural killer (NK) cells at the expense of B and T cells. Single cell RNA and ATAC-sequencing revealed that lineage skewing manifested early within hematopoietic progenitors. Further, knockout of TRIM28 or EHMT1 generated NK cells with distinct effector functions, where loss of TRIM28 resulted in enhanced IFN-ɣ producing NK cells and loss of EHMT1 enhanced the generation of CD16+ NK cells. Distinct TE families were epigenetically derepressed in EHMT1 versus TRIM28 knockout NK cells, yet enriched for NK-relevant transcription factor motifs. Modulation of heterochromatin machinery underscores the role of TEs in human hematopoietic differentiation and enables novel approaches to derive diverse NK cell subtypes for adoptive cell therapies.
2024-05-31 | GSE232101 | GEO
Project description:East African cichlid fishes have radiated in an explosive fashion. The (epi)genetic basis for the abundant phenotypic diversity of these fishes remains largely unknown. As transposable elements (TEs) contribute extensively to genome evolution, we reasoned that TEs may have fuelled cichlid radiations. While TE-derived genetic and epigenetic variability has been associated with phenotypic traits, TE expression and epigenetic silencing remain unexplored in cichlids. Here, we profiled TE expression in African cichlids, and describe dynamic expression patterns during embryogenesis and according to sex. Most TE silencing factors are conserved and expressed in cichlids. We describe an expansion of two truncated Piwil1 genes in Lake Malawi/Nyasa cichlids, encoding a Piwi domain with catalytic potential. To further dissect epigenetic silencing of TEs, we focused on small RNA-driven epigenetic silencing. We detect a small RNA population in gonads consistent with an active Piwi-interacting RNA (piRNA) pathway targeting TEs. We uncover fluid genomic origins of piRNAs in closely related cichlid species. This, along with signatures of positive selection in piRNA pathway factors, points towards fast co-evolution of TEs and the piRNA pathway. Our study is the first step to understand the contribution of ongoing TE-host arms races to the cichlid radiations in Africa.
2024-04-02 | PXD047439 | Pride
Project description:The diversity of small RNA-directed DNA methylation (RdDM) mechanisms have been underestimated due to the nearly complete transcriptional silencing of transposable elements (TEs) in the wild-type reference strains of Arabidopsis thaliana. In plants mutant for the SWI/SNF histone remodeler DDM1, TEs are globally activated due to loss of genome wide heterochromatin condensation. Transcriptionally activated TEs go through additional non-canonical forms of RdDM that are dependent on RNA Polymerase II expression. However, the global targets of the non-canonical RdDM pathway have not been explored. In an attempt to identify and contrast the targets of canonical and expression-dependent non-canonical RdDM, we performed MethylC-seq of genome-wide DNA methylation patterns from several RdDM mutants in either the TE-silent or the TE-active (ddm1) contexts. Arabidopsis wildtype and twenty RdDM pathway mutants
2016-07-22 | E-GEOD-79746 | biostudies-arrayexpress
Project description:Transposable elements (TEs) appear to have contributed to the evolution of tissue-specific gene regulatory networks in contexts such as early development, pregnancy and innate immunity, amongst others. In mouse embryonic stem cells (ESCs), TE families such as RLTR13D6 bind key pluripotency-associated transcription factors and are enriched for histone marks that are characteristic of distal enhancers. However, it remains unclear to what extent such lineage-specific TEs are important for maintaining gene expression programmes during preimplantation development. Here we have tested the gene regulatory function of RLTR13D6 elements in ESCs using epigenetic editing approaches. Whilst we identify some elements that are important to drive gene expression, these constitute a minority of all the putative TE-derived enhancers identified through epigenomic analyses, highlighting the importance of functional tests when assessing the contribution of TEs to gene regulatory networks.
2018-12-18 | GSE122855 | GEO