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Active endogenous retroviral elements in human pluripotent stem cells are functional in regulating host gene expression

ABSTRACT: Active endogenous retroviral elements in human pluripotent stem cells are functional in regulating host gene expression

PROVIDER: PRJNA773772 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16538250_1.fastq.gz	Fastqsanger.gz
	SRR16538250_2.fastq.gz	Fastqsanger.gz
	SRR16538251_1.fastq.gz	Fastqsanger.gz
	SRR16538251_2.fastq.gz	Fastqsanger.gz
	SRR16538252_1.fastq.gz	Fastqsanger.gz

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Endogenous retroviral elements of CHO cells

Project description:Endogenous retroviral elements of CHO cells

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Active endogenous retroviral elements in human pluripotent stem cells are functional in regulating host gene expression

Project description:Human endogenous retroviruses were also called LTR elements which can be bound by transcription factors and marked by different histone modifications. In previous studies, LTR had been considered harmful to genome stability, but recently individual LTR or certain subclasses of LTRs such as LTR7/HERVH and LTR5/HERVK families had been identified as functional elements which had acted as a cis-regulatory element, constructed topological domains and contributed to immunity. However, there were still many LTR elements with unknown functions, and the biological significance of LTR for the host was poorly understood. Overall, our study has not only provided a comprehensive regulatory map of LTRs in human ESCs, but also explored the regulatory models of MER57E3 and LTR5_Hs on host genes.

2022-04-01 | GSE186430 | GEO

Active endogenous retroviral elements in human pluripotent stem cells play a role in regulating host gene expression.

Project description:Human endogenous retroviruses, also called LTR elements, can be bound by transcription factors and marked by different histone modifications in different biological contexts. Recently, individual LTR or certain subclasses of LTRs such as LTR7/HERVH and LTR5_Hs/HERVK families have been identified as cis-regulatory elements. However, there are still many LTR elements with unknown functions. Here, we dissected the landscape of histone modifications and regulatory map of LTRs by integrating 98 ChIP-seq data in human embryonic stem cells (ESCs), and annotated the active LTRs enriching enhancer/promoter-related histone marks. Notably, we found that MER57E3 functionally acted as proximal regulatory element to activate respective ZNF gene. Additionally, HERVK transcript could mainly function in nucleus to activate the adjacent genes. Since LTR5_Hs/LTR5 was bound by many early embryo-specific transcription factors, we further investigated the expression dynamics in different pluripotent states. LTR5_Hs/LTR5/HERVK exhibited higher expression level in naïve ESCs and extended pluripotent stem cells (EPSCs). Functionally, the LTR5_Hs/LTR5 with high activity could serve as a distal enhancer to regulate the host genes. Ultimately, our study not only provides a comprehensive regulatory map of LTRs in human ESCs, but also explores the regulatory models of MER57E3 and LTR5_Hs/LTR5 in host genome.

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SOX2 Reprograms the Esophageal Squamous Carcinoma Epigenome and Induces Endogenous Retroviral Elements and dsRNA, Thereby Promoting ADAR1 Dependence

Project description:SOX2 Reprograms the Esophageal Squamous Carcinoma Epigenome and Induces Endogenous Retroviral Elements and dsRNA, Thereby Promoting ADAR1 Dependence

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TIP60 represses activation of endogenous retroviral elements

Project description:We found that the loss of TIP60 de-represses retrotransposon elements genome-wide, which in turn activate the cellular response to pathogens mediated by STING, culminating in an induction of Interferon Regulatory Factor 7 (IRF7) and associated inflammatory response.

2019-12-01 | GSE108834 | GEO

SOX2 Reprograms the Esophageal Squamous Carcinoma Epigenome and Induces Endogenous Retroviral Elements and dsRNA, Thereby Promoting ADAR1 Dependence [RNA-Seq]

Project description:SOX2 Reprograms the Esophageal Squamous Carcinoma Epigenome and Induces Endogenous Retroviral Elements and dsRNA, Thereby Promoting ADAR1 Dependence [RNA-Seq]

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Suppression of endogenous retroviral enhancers in somatic cell nuclear transfer embryos

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Endogenous retroviral insertions drive non-canonical imprinting in extra-embryonic tissues

Project description:Endogenous retroviral insertions drive non-canonical imprinting in extra-embryonic tissues

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TIP60 represses activation of endogenous retroviral elements.

Project description:TIP60 is a lysine acetyltransferase and is known to be a haplo-insufficient tumor suppressor. TIP60 downregulation is an early event in tumorigenesis which has been observed in several cancer types including breast and colorectal cancers. However, the mechanism by which it regulates tumor progression is not well understood. In this study, we identified the role of TIP60 in the silencing of endogenous retroviral elements (ERVs). TIP60-mediated silencing of ERVs is dependent on BRD4. TIP60 and BRD4 positively regulate the expression of enzymes, SUV39H1 and SETDB1 and thereby, the global H3K9 trimethylation (H3K9me3) level. In colorectal cancer, we found that the loss of TIP60 de-represses retrotransposon elements genome-wide, which in turn activate the cellular response to pathogens, mediated by STING, culminating in an induction of Interferon Regulatory Factor 7 (IRF7) and associated inflammatory response. In summary, this study has identified a unique mechanism of ERV regulation in cancer cells mediated by TIP60 and BRD4 through regulation of histone H3 K9 trimethylation, and a new tumor suppressive role of TIP60 in vivo.

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Loss of Uhrf1 in neural stem cells leads to activation of retroviral elements and delayed neurodegeneration [E16]

Project description:In order to understand if early epigenetic mechanisms instruct the long-term behaviour of neural stem cells (NSCs) and their progeny, we examined the protein Uhrf1 as it is highly expressed in NSCs of the developing brain and rapidly downregulated upon differentiation. Conditional deletion of Uhrf1 in the developing cerebral cortex resulted in rather normal proliferation and neurogenesis but severe postnatal neurodegeneration. During development, deletion of Uhrf1 resulted in global DNA hypomethylation with a strong activation of the IAP family of endogenous retroviral elements, accompanied by an increase in hydroxy methyl cytosine. Downregulation of Tet enzymes rescued the IAP activation in Uhrf1 cKO cells, suggesting an antagonistic interplay between Uhrf1 and Tet on IAP regulation. As IAP upregulation persists into postnatal stages in the conditional Uhrf1 KO mice, our data show the lack of means to repress IAPs in differentiating neurons that normally never express Uhrf1. The high load of viral proteins and other transcriptional dysregulation ultimately lead to extensive postnatal neurodegeneration. Taken together, these data show that early developmental NSC factors can have long-term effects in neuronal differentiation and survival. Moreover, it highlights how specific the consequences of widespread changes in DNA methylation are for certain classes of retroviral elements.

2016-11-01 | GSE84545 | GEO

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