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Epigenomic conservation of transposable element silencing

ABSTRACT: Epigenomic conservation of transposable element silencing

OTHER RELATED OMICS DATASETS IN: GSE96710GSE96712GSE96711

PROVIDER: PRJNA379439 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14873182_1.fastq.gz	Fastqsanger.gz
	SRR14873182_2.fastq.gz	Fastqsanger.gz
	SRR14873183_1.fastq.gz	Fastqsanger.gz
	SRR14873183_2.fastq.gz	Fastqsanger.gz
	SRR14873184_1.fastq.gz	Fastqsanger.gz

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Epigenomic conservation of transposable element silencing [ChIP-seq]

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Epigenomic conservation of transposable element silencing [RNA-seq]

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Epigenomic conservation of transposable element silencing [RNA-seq]

Project description:Transposable elements (TEs) comprise a substantial proportion of primate genomes. Because of the potential deleterious effects of TEs during development, TEs are targeted for silencing by sequence-specific KRAB-ZNF proteins, which recruit the TRIM28-SETDB1 complex, to deposit the repressive histone modification H3K9me3. TEs, in turn, acquire mutations to evade detection by the host, and hence KRAB-ZNF proteins need to rapidly evolve to counteract them. To investigate the short-term evolution of TE silencing, we profiled the genome-wide distribution of H3K9me3 in both human and chimpanzee induced pluripotent stem cells. We performed chromatin immunoprecipitation followed by high-throughput sequencing for H3K9me3, as well as total RNA sequencing in ten human and seven chimpanzee individuals. H3K9me3 enrichment was quantified in 141,642 regions determined to be orthologous between the two species. These H3K9me3-enriched regions were overlaid on a compiled set of 4 million orthologous TEs that can be mapped in both species.

2018-04-26 | GSE96711 | GEO

Epigenomic conservation of transposable element silencing [ChIP-seq]

2018-04-26 | GSE96710 | GEO

Epigenomic conservation of transposable element silencing

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-04-25 | GSE96712 | GEO

Small RNA accumulation in Transposable Element-silent and Transposable Element-active epigenomes

Project description:Background: The small RNAs that Transposable Elements generate are vastly different when they are transcriptionally silenced compared to when they are transcriptionally activated. We performed the deep sequencing of small RNAs in a number of small RNA biogenesis mutants in both Transposable Element-silenced and Transposable Element-active epigenome backgrounds. Results: We found that Transposable Elements generate large amounts of 21-22nt siRNAs only when they are transcriptionally active. These 21-22nt siRNAs are incorporated into the AGO6 protein. Conclusion: Ago6 is the key protein that bridges the post-transcriptional degradation of Transposable Element mRNAs and the establishment of DNA methylation. Examination of flower bud small RNAs from wild type and 5 single or double mutant combinations, many of which have biological replicates. In addition, IP purification of the AGO6 protein (and mock no-antigen controls) followed by sequencing of the incorporated small RNAs. Replicate A for Col and ddm1 are submitted in GSE41755

2014-11-14 | E-GEOD-57191 | biostudies-arrayexpress

MicroRNA-dependent transposable element transcriptional silencing in Drosophila somatic ovarian cells

Project description:MicroRNA-dependent transposable element transcriptional silencing in Drosophila somatic ovarian cells

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Small RNA accumulation in Transposable Element-silent and Transposable Element-active epigenomes

2014-11-14 | GSE57191 | GEO

Incorporation of transposable element small RNAs into the Arabidopsis AGO1 protein

Project description:Background: Transposable element 24 nucleotide small RNAs are not efficiently incorporated into the AGO1 protein, which is involved in endogenous RNAi and gene regulation through the microRNA and tasiRNA pathways. Results: The AGO1 protein incorporates large quantities of transposable element siRNAs when transposable elements are epigenetically activated and transcribed. The incorporation of transposable element siRNAs is at the expense of the most abundant microRNAs. These transposable element siRNAs can act as tasiRNAs, regulating genes that they have partial complementarity to. Conclusion: Transposable element small RNAs are more dynamic than previously thought. They can be incorporated into AGO1 and regulate genes. Three biological replicates of small RNA sequencing from two genotypes

2014-04-07 | E-GEOD-45990 | biostudies-arrayexpress

Pathogenic tau-induced piRNA depletion promotes neuronal death through transposable element dysregulation in neurodegenerative tauopathies

Project description:Transposable elements, known colloquially as “jumping genes,” constitute approximately 45% of the human genome. Cells utilize epigenetic defenses to limit transposable element jumping, including formation of silencing heterochromatin and generation of piwi-interacting RNAs (piRNAs), small RNAs that facilitate clearance of transposable element transcripts. Here we identify transposable element activation as a key mediator of neuronal death in tauopathies, a group of neurodegenerative disorders, including Alzheimer’s disease, that are pathologically characterized by deposits of tau protein in the brain. Mechanistically, we find that heterochromatin decondensation and reduction of piwi/piRNAs drive transposable element activation in tauopathy. Using genetic and pharmacological approaches in a Drosophila melanogaster model of tauopathy, we provide evidence for a causal relationship between pathogenic tau-induced heterochromatin decondensation, piwi/piRNA depletion, active transposable element obilization, and neurodegeneration. We further report a significant increase in transcripts of the endogenous retrovirus class of transposable elements in human Alzheimer’s disease and progressive supranuclear palsy, suggesting that transposable element dysregulation is conserved in human tauopathy. Taken together, our data identify heterochromatin decondensation, piwi/piRNA depletion and consequent transposable element activation as a novel, pharmacologically targetable, mechanistic driver of neurodegeneration in tauopathy.

2018-07-04 | GSE115606 | GEO

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