Transposons repressed by H3K27me3 were co-opted as cis-regulatory elements of H3K27me3 controlled protein-coding genes during evolution of plants
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PROVIDER: PRJNA915099 | ENA |
REPOSITORIES: ENA
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Project description:This SuperSeries is composed of the SubSeries listed below.
2023-09-21 | GSE221635 | GEO
Project description:Co-opted transposons help perpetuate conserved higher-order chromosomal structures
| PRJNA593858 | ENA
Project description:Domestication of transposable elements (TEs) into functional cis-regulatory elements is a widespread phenomenon. However, why some TEs are co-opted as functional enhancers while others are not is underappreciated. SINE-Vntr-Alus (SVAs) are the youngest group of transposons in the human genome, where ~3,700 copies are annotated, nearly half of which are human-exclusive. Many studies indicated that the SVAs are among the most frequently co-opted TEs in human gene regulation, but the mechanisms underlying such process have not yet been thoroughly investigated. Here, we leveraged CRISPR-interference (CRISPRi), computational and functional genomics to elucidate the genomic features that underlie SVA domestication into human stem-cell gene regulation. We found that ~750 SVAs are co-opted as functional cis-regulatory elements in human induced Pluripotent Stem Cells. Co-opted SVAs are significantly closer to genes and harbor more transcription factor binding sites than the not co-opted ones. We show that a long DNA-motif composed of flanking YY1/2 and OCT4 binding sites is enriched in the co-opted SVAs, and that these two factors bind, as predicted, near each other on the TE sequence. Repression of all the ~750 co-opted SVAs by CRISPRi in a line with stem-like properties (NCCIT) led to loss of YY1/OCT4 binding and alteration of neighboring gene expression. Ultimately, SVA repression resulted in ~3,000 differentially expressed genes, 131 of which were the nearest gene to an annotated SVA. In summary, we demonstrated that SVAs contribute significantly to human gene regulation, and that both genomic location and sequence composition contribute to SVA domestication in the gene regulatory networks.
2022-01-04 | GSE192951 | GEO
Project description:BackgroundTransposable elements (TEs) make up half of mammalian genomes and shape genome regulation by harboring binding sites for regulatory factors. These include binding sites for architectural proteins, such as CTCF, RAD21, and SMC3, that are involved in tethering chromatin loops and marking domain boundaries. The 3D organization of the mammalian genome is intimately linked to its function and is remarkably conserved. However, the mechanisms by which these structural intricacies emerge and evolve have not been thoroughly probed.ResultsHere, we show that TEs contribute extensively to both the formation of species-specific loops in humans and mice through deposition of novel anchoring motifs, as well as to the maintenance of conserved loops across both species through CTCF binding site turnover. The latter function demonstrates the ability of TEs to contribute to genome plasticity and reinforce conserved genome architecture as redundant loop anchors. Deleting such candidate TEs in human cells leads to the collapse of conserved loop and domain structures. These TEs are also marked by reduced DNA methylation and bear mutational signatures of hypomethylation through evolutionary time.ConclusionsTEs have long been considered a source of genetic innovation. By examining their contribution to genome topology, we show that TEs can contribute to regulatory plasticity by inducing redundancy and potentiating genetic drift locally while conserving genome architecture globally, revealing a paradigm for defining regulatory conservation in the noncoding genome beyond classic sequence-level conservation.
| S-EPMC6979391 | biostudies-literature
Project description:Genome wide chromatin maps have shown that spreading repressive histone modifications such as H3K9me3 and H4K20me3 are present on pericentromeric and telomeric repeats and on the inactive X chromosome where H3K27me3 or H3K9me3 alternately modify megabasepair sized domains. However, only a few regions along an autosome of which Homeobox gene clusters are notable examples, have been shown to display spreading of repressive histone modifications. Here we present a ChIP-Chip map of repressive and active histone modifications along mouse Chr.17 in embryonic, fibroblast cells. Our results show that the majority of H3K27me3 modifications form BLOCs rather than focal peaks. H3K27me3 BLOCs modify silent genes of all types and their flanking intergenic regions, indicating a negative correlation between H3K27me3 and transcription. However, non-transcribed gene-poor regions also lacked H3K27me3. We therefore performed a low resolution analysis of whole mouse Chr.17 which revealed that H3K27me3 specifically marks megabasepair sized domains that are enriched for genes, SINEs and active histone modifications. These genic H3K27me3 domains alternate with similar sized gene-poor domains that are deficient in active histone modifications, but enriched for LINE and LTR transposons as well as H3K9me3 and H4K20me3. Thus, a mouse autosome can be seen to contain alternating chromatin bands that predominantly separate genes from one retrotransposons class, which could offer unique chromatin compartments for the specific regulation of genes or the silencing of transposons. mapping of H3K27me3 histone modification in one MEF cell line (MEFF)
2008-12-22 | E-GEOD-12721 | biostudies-arrayexpress
Project description:Genome wide chromatin maps have shown that spreading repressive histone modifications such as H3K9me3 and H4K20me3 are present on pericentromeric and telomeric repeats and on the inactive X chromosome where H3K27me3 or H3K9me3 alternately modify megabasepair sized domains. However, only a few regions along an autosome of which Homeobox gene clusters are notable examples, have been shown to display spreading of repressive histone modifications. Here we present a ChIP-Chip map of repressive and active histone modifications along mouse Chr.17 in embryonic, fibroblast cells. Our results show that the majority of H3K27me3 modifications form BLOCs rather than focal peaks. H3K27me3 BLOCs modify silent genes of all types and their flanking intergenic regions, indicating a negative correlation between H3K27me3 and transcription. However, non-transcribed gene-poor regions also lacked H3K27me3. We therefore performed a low resolution analysis of whole mouse Chr.17 which revealed that H3K27me3 specifically marks megabasepair sized domains that are enriched for genes, SINEs and active histone modifications. These genic H3K27me3 domains alternate with similar sized gene-poor domains that are deficient in active histone modifications, but enriched for LINE and LTR transposons as well as H3K9me3 and H4K20me3. Thus, a mouse autosome can be seen to contain alternating chromatin bands that predominantly separate genes from one retrotransposons class, which could offer unique chromatin compartments for the specific regulation of genes or the silencing of transposons.
2008-12-22 | GSE12721 | GEO
Project description:SINE transposons in multiple lepidopteran insects Raw sequence reads
| PRJNA665855 | ENA
Project description:The piRNA pathway controls transposon expression in animal germ cells, thereby ensuring genome stability over generations. piRNAs are maternally deposited and required for proper transposon silencing in adult offspring. However, a long-standing question in the field is the precise function of maternally deposited piRNAs and its associated factors during embryogenesis. Here, we probe the spatio-temporal expression patterns of several piRNA pathway components during early stages of development. Amongst those, factors required for transcriptional gene silencing (TGS) showed ubiquitous abundance in somatic and pole cells throughout the first half of embryogenesis. We further analysed the transcriptomes of various embryo stages and correlated these with the presence of selected chromatin marks. We found that a number of transposon families show bursts of transcription during early embryonic stages. Transposons heavily targeted by maternally deposited piRNAs accumulated repressive chromatin marks following their spike in expression. Furthermore, depletion of maternally deposited Piwi protein in early embryos resulted in increased expression of transposons targeted by inherited piRNAs and was accompanied by a strong loss of repressive chromatin marks at coding sequences. Overall, our data suggests a pivotal role for the piRNA pathway in transposon defence during Drosophila embryogenesis in somatic cells.
2021-07-26 | PXD022409 | Pride
Project description:The role that gamete-inherited chromatin states serve in regulating gene expression across generations is poorly understood. To interrogate how histone marks inherited on parental genomes influence gene expression in offspring, we profiled different tissue contexts in worms that inherited the sperm genome lacking the repressive mark H3K27me3. We found that worms that inherited the sperm genome lacking H3K27me3 upregulated genes in all tissues profiled, which included hermaphrodite and male germlines and mixed soma. We found that most upregulated genes were upregulated specifically from sperm alleles and in a tissue-specific manner, highlighting the importance of cellular context in determining which genes are sensitive to upregulation when H3K27me3 repression is absent. To determine whether chromatin states can impact gene expression transgenerationally, i.e. across 3 generations, we profiled gene expression and chromatin states in the germlines of worms that inherited the sperm genome lacking H3K27me3 (F1 generation) and in the germlines of their offspring (F2 generation). We found that genes upregulated in F1 germlines maintained the H3K27me3(-) state of sperm alleles and that the upregulated and H3K27me3(-) state of sperm alleles was maintained in the germlines of their offspring (F2 generation). These findings demonstrate that histone marks can serve as a transgenerational carrier.
2022-05-31 | GSE205113 | GEO
Project description:Suppression of polycomb-mediated H3K27me3 epigenetically de-repressed the genome-wide expression of effectomes in the vegetative growth stage
| PRJNA701612 | ENA