Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transposable elements as lineage-specific enhancers in endodermal-lineage cancers (ChIP-Seq)

ABSTRACT: Transposable elements (TE) are repetitive genomic elements that harbor binding sites for human transcription factors (TF). A regulatory role for TEs has been suggested in embryonal development and diseases such as cancer but systematic investigation of their functions has been limited by their widespread silencing in the genome. Here, we have utilized unbiased massively parallel reporter assay data using whole human genome library to identify TEs with functional enhancer activity in two human cancer types of endodermal lineage, colorectal and liver cancers. We show that the identified TE enhancers are characterized by genomic features associated with active enhancers, such as epigenetic marks and TF binding. Importantly, we identified distinct TE subfamilies that function as tissue-specific enhancers, namely MER11- and LTR12-elements in colon and liver cancers, respectively. These elements are bound by distinct TFs in each cell type, and they have predicted associations to differentially expressed genes. In conclusion, these data demonstrate how different cancer types can utilize distinct TEs as tissue-specific enhancers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE221046 | GEO | 2023/08/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transposable elements as lineage-specific enhancers in endodermal-lineage cancers [NaNoME-seq]

Project description:Transposable elements (TE) are repetitive genomic elements that harbor binding sites for human transcription factors (TF). A regulatory role for TEs has been suggested in embryonal development and diseases such as cancer but systematic investigation of their functions has been limited by their widespread silencing in the genome. Here, we have utilized unbiased massively parallel reporter assay data using whole human genome library to identify TEs with functional enhancer activity in two human cancer types of endodermal lineage, colorectal and liver cancers. We show that the identified TE enhancers are characterized by genomic features associated with active enhancers, such as epigenetic marks and TF binding. Importantly, we identified distinct TE subfamilies that function as tissue-specific enhancers, namely MER11- and LTR12-elements in colon and liver cancers, respectively. These elements are bound by distinct TFs in each cell type, and they have predicted associations to differentially expressed genes. In conclusion, these data demonstrate how different cancer types can utilize distinct TEs as tissue-specific enhancers.

2023-08-11 | GSE224453 | GEO

Transposable elements as lineage-specific enhancers in endodermal-lineage cancers (STARR-Seq)

2023-08-11 | GSE221045 | GEO

Transposable elements as lineage-specific enhancers in endodermal-lineage cancers (ATAC-Seq)

2023-08-11 | GSE221051 | GEO

Transposable elements as lineage-specific enhancers in endodermal-lineage cancers (RNA-Seq)

2023-08-11 | GSE221050 | GEO

Transposable elements as lineage-specific enhancers in endodermal-lineage cancers (Hi-ChIP-Seq)

2023-08-11 | GSE221052 | GEO

Widespread contribution of transposable elements to the innovation of gene regulatory networks [human ENCODE]

Project description:Transposable elements (TE) have been shown to contrain functional transcription factor (TF) binding sites for long, but the extent to which TEs contribute TF binding sites is not well know. Here, we comprehensively mapped binding sites for 26 pairs of orthologous TFs, in two pairs of human and mouse cell lines (i.e., leukemia, and lymphoblast), along with epigenomic profiles representing DNA methylation and six histone modifications. We found that on average, 20% of TF binding sites were embedded in TEs. We further identified 710 TF-TE relationships in which certain TE subfamilies enriched for TF binidng sites. TE-derived TF binding peaks were also strongly associated with decreased DNA methylation and increased enhancer-associated histone marks. Most of the TE-derived TF binding sites were species-specific, but we also identified conserved binding sites. Additionally, 66% of TE-derived TF binding events were cell-type specific, associated with cell-type specific epigenetic landscape. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf To evaluate the contribution of transposable elements (TE) to transcription factor (TF) binding landscapes, we profiled ChIP-seq datasets for 26 TFs in two cell lines in human and mouse, generated by the ENCODE and MouseENCODE consortia. The epigenomic profiles were evaluated from six histone modification in each of the cell lines, also generated by the consortia. We added DNA methylation to the epigenomic profiles, using two complementary techniques, MeDIP-seq and MRE-seq. The mouse data related to this study are available through GSE57230: http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE57230

2014-05-09 | E-GEOD-56774 | biostudies-arrayexpress

Widespread contribution of transposable elements to the innovation of gene regulatory networks [mouse ENCODE]

Project description:Transposable elements (TE) have been shown to contrain functional transcription factor (TF) binding sites for long, but the extent to which TEs contribute TF binding sites is not well know. Here, we comprehensively mapped binding sites for 26 pairs of orthologous TFs, in two pairs of human and mouse cell lines (i.e., leukemia, and lymphoblast), along with epigenomic profiles representing DNA methylation and six histone modifications. We found that on average, 20% of TF binding sites were embedded in TEs. We further identified 710 TF-TE relationships in which certain TE subfamilies enriched for TF binidng sites. TE-derived TF binding peaks were also strongly associated with decreased DNA methylation and increased enhancer-associated histone marks. Most of the TE-derived TF binding sites were species-specific, but we also identified conserved binding sites. Additionally, 66% of TE-derived TF binding events were cell-type specific, associated with cell-type specific epigenetic landscape. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf To evaluate the contribution of transposable elements (TE) to transcription factor (TF) binding landscapes, we profiled ChIP-seq datasets for 26 TFs in two cell lines in human and mouse, generated by the ENCODE and MouseENCODE consortia. The epigenomic profiles were evaluated from six histone modification in each of the cell lines, also generated by the consortia. We added DNA methylation to the epigenomic profiles, using two complementary techniques, MeDIP-seq and MRE-seq. The human data related to this study are available through GSE56774: http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE56774

2014-05-09 | E-GEOD-57230 | biostudies-arrayexpress

ZFP462 safeguards neural lineage specification by targeting G9A/GLP-mediated heterochromatin to silence enhancers

Project description:ZNF462 haploinsufficiency is linked to Weiss-Kruszka Syndrome, a genetic disorder characterized by neurodevelopmental defects including Autism. Though conserved in vertebrates and essential for embryonic development the molecular functions of ZNF462 remain unclear. We identified its murine homolog ZFP462 in a screen for mediators of epigenetic gene silencing. Here, we show that ZFP462 safeguards neural lineage specification of mouse embryonic stem cells (ESCs) by targeting the H3K9-specific histone methyltransferase complex G9A/GLP to silence mesoendodermal genes. ZFP462 binds to transposable elements (TEs) that are potential enhancers harboring ESC-specific transcription factor (TF) binding sites. Recruiting G9A/GLP, ZFP462 seeds heterochromatin, restricting TF binding. Loss of ZFP462 in ESCs results in increased chromatin accessibility at target sites and ectopic expression of mesoendodermal genes. Taken together, ZFP462 confers lineage- and locus-specificity to the broadly expressed epigenetic regulator G9A/GLP. Our results suggest that aberrant activation of lineage non-specific genes in the neuronal lineage underlies ZNF462-associated neurodevelopmental pathology.

2023-05-10 | PXD037238 | Pride

Evolutionary rewiring of wheat abiotic stress responsive network by lineage-specific transposable elements I

Project description:The yield of wheat is highly impacted by environmental stresses. The combinatorial regulation of sequence-specific transcription factors(TFs) defines a regulatory network that underlies plant stress responses. Here we created a comprehensive catalog of genomic binding sites of 115 TFs underlying abiotic stress responses by leveraging DAP-seq in Triticum Urartu, along with epigenomic profiles. The majority of gene distant TF binding sites(TFBS) are embedded in transposable elements(TEs), whose functional relevance was supported by a signature of purifying selection and active epigenomic features. Furthermore, ~30% non-TE TFBS share high sequence similarity with TE-embeded TFBS, potentially derived from Triticeae-specific TEs and have almost no sequence homology in non-Triticeae species. The expansion of TE-derived TFBS in wheat linked to wheat-specific stress responsive genes, suggesting that TEs are an important driving force for regulatory innovation. Altogether, TEs have significantly and continuously shaped regulatory network in wheat adaptation.

2021-08-31 | GSE167228 | GEO

Evolutionary rewiring of wheat abiotic stress responsive network by lineage-specific transposable elements [ChIP-Seq]

2021-08-31 | GSE182693 | GEO