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Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [DNase-Seq]

ABSTRACT: Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [DNase-Seq]

PROVIDER: PRJNA563620 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10059493_1.fastq.gz	Fastqsanger.gz
	SRR10059493_2.fastq.gz	Fastqsanger.gz
	SRR10059494_1.fastq.gz	Fastqsanger.gz
	SRR10059494_2.fastq.gz	Fastqsanger.gz
	SRR10059495_1.fastq.gz	Fastqsanger.gz

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Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia

Project description:Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia

| PRJNA563616 | ENA

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [DNase-Seq]

Project description:Endogenous retroviruses (ERVs) and other transposons can act as tissue-specific regulators of gene expression in cis, with potential to affect biological processes. In cancer, epigenetic alterations and transcription factor misregulation may uncover the regulatory potential of typically repressed ERVs, which could contribute to tumour evolution and progression. Here, we asked whether transposons help to rewire oncogenic transcriptional circuits in acute myeloid leukaemia (AML). Using epigenomic data from both primary cells and cell lines, we have identified six ERV families that are frequently found in an open chromatin state in AML when compared to differentiated myeloid cells. A subset of these AML-associated ERVs harbour enhancer-specific histone modifications, and are bound by transcription factors that play key roles in haematopoiesis and in the pathogenesis of AML. Using CRISPR-mediated genetic and epigenetic editing, we have established causal links between ERV deregulation in AML and expression changes of adjacent genes. Finally, we show that deletion and epigenetic silencing of an ERV associated with the APOC1 gene leads to growth suppression by inducing apoptosis in leukemia cell lines. Our results suggest that ERV derepression provides an additional layer of gene regulation in AML that may be exploited by cancer cells to help drive oncogenic phenotypes.

2019-09-04 | GSE136760 | GEO

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [ChIP-Seq]

Project description:Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [ChIP-Seq]

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Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [RNA-Seq]

Project description:Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [RNA-Seq]

| PRJNA563622 | ENA

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [ChIP-Seq]

2019-09-04 | GSE136759 | GEO

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [RNA-Seq]

2019-09-04 | GSE136763 | GEO

Endogenous retroviruses are a source of enhancers with oncogenic potential in acute myeloid leukaemia.

Project description:Acute myeloid leukemia (AML) is characterised by a series of genetic and epigenetic alterations that result in deregulation of transcriptional networks. One understudied source of transcriptional regulators are transposable elements (TEs), whose aberrant usage could contribute to oncogenic transcriptional circuits. However, the regulatory influence of TEs and their links to AML pathogenesis remain unexplored. Here we identify six endogenous retrovirus (ERV) families with AML-associated enhancer chromatin signatures that are enriched in binding of key regulators of hematopoiesis and AML pathogenesis. Using both locus-specific genetic editing and simultaneous epigenetic silencing of multiple ERVs, we demonstrate that ERV deregulation directly alters the expression of adjacent genes in AML. Strikingly, deletion or epigenetic silencing of an ERV-derived enhancer suppresses cell growth by inducing apoptosis in leukemia cell lines. This work reveals that ERVs are a previously unappreciated source of AML enhancers that may be exploited by cancer cells to help drive tumour heterogeneity and evolution.

| S-EPMC7360734 | biostudies-literature

Endogenous retroviruses act as enhancers to drive species-specific germline transcriptomes in mammals

Project description:Gene regulation in the germline ensures the production of high-quality gametes, long-term maintenance of the species, and speciation. Germline transcriptomes undergo dynamic changes after the mitosis-to-meiosis transition in males and have been subject to evolutionary divergence among mammals. However, the mechanism that underlies germline regulatory divergence remains undetermined. Here, we show that endogenous retroviruses influence species-specific germline transcriptomes in mammals. We show that the endogenous retroviruses function as active enhancers to drive evolutionarily young (mouse or rodent specific) spermatogenesis-specific genes after the mitosis-to-meiosis transition in male mice. These ERV loci bear binding motifs for critical regulators of spermatogenesis such as A-MYB. The genome-wide transposition of ERVs might have rewired germline gene expression in a species-specific manner. Notably, these features are present in human spermatogenesis, but independently evolved ERVs are associated with expression of germline genes, demonstrating the prevalence of ERV-driven mechanisms in mammals. Together, we propose a model whereby species-specific transcriptomes are fine-tuned by endogenous retroviruses in the mammalian germline.

2020-05-28 | GSE142173 | GEO

Hijacking of transcriptional condensates by endogenous retroviruses

Project description:Hijacking of transcriptional condensates by endogenous retroviruses

| PRJNA669013 | ENA

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia

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

2019-09-04 | GSE136764 | GEO