Ontology highlight
ABSTRACT:
PROVIDER: PRJNA647441 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12272956.fastq.gz | Fastqsanger.gz | |||
| SRR12272957_1.fastq.gz | Fastqsanger.gz | |||
| SRR12272957_2.fastq.gz | Fastqsanger.gz |
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Project description:Chromatin is divided into euchromatin and heterochromatin based on differential compaction during interphase, with heterochromatin being highly condensed, existing in transcriptional inert conformation. Embedded within heterochromatin is a group of highly repetitive DNA sequences, referred to as satellite DNAs that give rise to non-coding satellite RNAs. Satellite DNA is thought to be maintained in a transcriptionally silenced state by the repressive H3K9me3 mark. However, aberrant satellite transcription can cause heterochromatin disorganization and genome instability, which have been linked to carcinogenesis. In order to study the function of heterochromatic satellite in retinal pigmental epithelia (RPE) cell, we systematically investigated transcriptome alterations in the presence of heterochromatin destabilization induced by satellite α overexpression in APRE19 cell line, a widely used human RPE cell line.
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Project description:Although heterochromatin is enriched with repressive traits, it is also actively transcribed, giving rise to large amounts of non-coding RNAs. Although these RNAs are responsible for the formation and maintenance of heterochromatin, little is known about how their transcription is regulated. Here we show that the Snail1 transcription factor represses pericentromeric transcription, acting through the H3K4 deaminase LOXL2. Since Snail1 plays a key role in the epithelial to mesenchymal transition (EMT), we analyzed the regulation of mouse heterochromatin transcription in this process. At the onset of EMT, one of the major structural heterochromatin proteins, HP1a, is transiently released from heterochromatin foci in a Snail1/LOXL2–dependent manner during EMT, concomitantly with a down-regulation of major satellite transcription. Global transcriptome analysis indicated that ectopic expression of heterochromatin transcripts affects the transcription profile of EMT-related genes. Additionally, preventing the down-regulation of major satellite transcripts compromised the migratory and invasive behavior of mesenchymal cells. We propose that Snail1 regulates heterochromatin transcription through the histone-modifying enzyme, LOXL2, thus creating the favorable transcriptional state necessary for completing EMT. Keywords: Expression Profiling by array We analyzed 2 arrays from each condition: Control and Major treated 8 hours with TGFbeta
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Project description:Many repetitive DNA elements are packaged in heterochromatin, but depend on occasional transcription to maintain long-term silencing. The factors that promote transcription of repeat elements in heterochromatin are largely unknown. Here, we show that DOT1L, a histone methyltransferase that modifies lysine 79 of histone H3 (H3K79), is required for transcription of major satellite repeats to maintain pericentromeric heterochromatin (PCH), and that this function is essential for preimplantation development. DOT1L is a transcriptional activator at single-copy genes but does not have a known role in repeat element transcription. We show that H3K79me3 is specifically enriched at repetitive elements, that loss of DOT1L compromises pericentromeric major satellite transcription, and that this function depends on interaction between DOT1L and the chromatin remodeler SMARCA5. DOT1L inhibition causes chromosome breaks and cell cycle defects, and leads to embryonic lethality. Together, our findings uncover a vital new role for DOT1L in transcriptional activation of heterochromatic repeats.
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Project description:Here, we analyzed two small RNA libraries derived from ovarian tissue mutant for either the Drosophila SETDB1 gene, or the Bam gene. Here we show that deposition of histone 3 lysine 9 by the methyltransferase dSETDB1 (egg) is required for piRNA cluster transcription. In the absence of dSETDB1, cluster precursor transcription collapses in germline and somatic gonadal cells and TEs are activated, resulting in germline loss and a block in germline stem cell differentiation. We propose that heterochromatin protects the germline by activating the piRNA pathway. Keyword : Epigenetics
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Project description:Here, we analyzed two small RNA libraries derived from ovarian tissue mutant for either the Drosophila SETDB1 gene, or the Bam gene. Here we show that deposition of histone 3 lysine 9 by the methyltransferase dSETDB1 (egg) is required for piRNA cluster transcription. In the absence of dSETDB1, cluster precursor transcription collapses in germline and somatic gonadal cells and TEs are activated, resulting in germline loss and a block in germline stem cell differentiation. We propose that heterochromatin protects the germline by activating the piRNA pathway. Keyword : Epigenetics 2 libraries were analyzed, with 1 being a developmental control (Bam Mutant).
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