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Strand-specific RNA-seq analysis after Ssrp1 knockout in embryonic stem cells

ABSTRACT: Endogenous retrovirus MERVL is specifically expressed in a minority of embryonic stem cells. To determine the restrain mechanism of MERVL, we knocked out Ssrp1 and analyzed the effect on the expression of transposable elements and coding genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE155863 | GEO | 2020/08/23

REPOSITORIES: GEO

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RNA-seq analysis after Ssrp1 knockout or Usp7 depletion in embryonic stem cells

Project description:Endogenous retrovirus MERVL is specifically expressed in a minority of embryonic stem cells. To determine the restrain mechanism of MERVL, we knocked out Ssrp1 and analyzed the effect on the expression of transposable elements and coding genes. Ssrp1 further interacts with ubiquitin specific protease Usp7. We knocked down usp7 and analyzed the effect on the expression of MERVL. It turns out the deletion of ssrp1 or usp7 would lead to upregulation of MERVL. This study extends our understandings of the machanism by novel factors regulates MERVL.

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Project description:Endogenous retroviruses (ERVs) were usually silenced by various histone modifications on histone H3 variants and respective histone chaperones in embryonic stem cells (ESCs). However, it is still unknown whether chaperones of other histones could repress ERVs. Here, we show that H2A/H2B histone chaperone FACT plays a critical role in silencing ERVs and ERV-derived cryptic promoters in ESCs. Loss of FACT component Ssrp1 activated MERVL whereas the re-introduction of Ssrp1 rescued the phenotype. Additionally, Ssrp1 interacted with MERVL and suppressed cryptic transcription of MERVL-fused genes. Remarkably, Ssrp1 interacted with and recruited H2B deubiquitinase Usp7 to Ssrp1 target genes. Suppression of Usp7 caused similar phenotypes as loss of Ssrp1. Furthermore, Usp7 acted by deubiquitinating H2Bub and thereby repressed the expression of MERVL-fused genes. Taken together, our study uncovers a unique mechanism by which FACT complex silences ERVs and ERV-derived cryptic promoters in ESCs.

2020-08-24 | PXD017351 | Pride

ChIP-seq analysis of Ssrp1 and Usp7 in mESCs

Project description:FACT was discovered to be a repressor of transcription in mES cells. In addition, the murine endogenous retrovirus were repressed by various mechanisms. Hence, we examined the possibility for Ssrp1 as a repressor of MT2/MERVL.

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RNA-seq analysis about MuERVL knocked down samples

Project description:Endogenous retrovirus MERVL is specifically expressed in a minority of embryonic stem cells and 2-cell embryos. To determine the function of MERVL transcripts, we knocked down MuERVL and analyzed the effect on the expression of MERVL and its targeting genes. It turns out the downregulation of MuERVL would lead to downregulation of MERVL nearby genes. This study extends our understandings of the machanism by which MERVL regulates its neatby genes.

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RNA-seq analysis about Pim-3 knocked out samples

Project description:Endogenous retroviruses (ERVs) are suppressed to maintain host genome stability and it’s regulatory mechanism remains unclear. To determine the restrain mechanism of MERVL, we knocked out Pim3 and analyzed the effect on the expression of transposable elements and coding genes. Our results show that Pim3 as a repressor of MERVL and 2-cell genes in ESCs. This study extends our understandings of the machanism by novel factors regulates MERVL.

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ChIP-seq for SSRP1

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Strand-specific RNA-seq analysis after Ssrp1 knockout in embryonic stem cells

Project description:Strand-specific RNA-seq analysis after Ssrp1 knockout in embryonic stem cells

| PRJNA655887 | ENA

ChIP-seq for SSRP1

Project description:ChIP-seq for SSRP1

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Murine Endogenous Retrovirus MERVL is essential for the transition from Totipotency to Pluripotency during Preimplantation Development

Project description:Zygotic genome activation (ZGA) is a critical post-fertilization step that promotes totipotency and allows different cell fates to emerge in the developing embryo. MERVL, murine endogenous retrovirus-L, is transiently upregulated at the 2-cell stage around the time of ZGA. Although MERVL expression is widely used as a marker of totipotency, the role of this retrotransposon in mouse embryogenesis remains elusive. Here, we develop methods for consistent knockdown (KD) and inactivation of interspersed copies of MERVL and show that MERVL transcripts, but not encoded retroviral proteins and their long terminal repeat (LTR) promoter that drives chimeric transcripts with host genes, is essential for accurate regulation of the host transcriptome and chromatin state during preimplantation development. Both KD and CRISPRi-based repression of MERVL result in embryonic lethality due to defects in differentiation and genomic stability. Furthermore, transcriptome and epigenome analysis revealed that loss of MERVL transcript led to retain an accessible chromatin state at, and aberrant expression of, a subset of 2-cell specific genes at mid-preimplantation stages. Taken together, our results suggest a model in which an endogenous retrovirus plays a critical role in regulating host cell fate potential.

2023-02-12 | GSE196520 | GEO

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