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Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (Hi-C)

ABSTRACT: Short interspersed nuclear element (SINE) B2 are a type of DNA retrotransposon that organize three-dimensional genome during development. Containing binding sites for CCCTC-binding factor (CTCF), SINE_B2 serve as domain boundary elements that control chromatin state and initiate transcription of critical developmental genes. However, it is still unclear how SINE_B2 are regulated during neurodevelopment. Our findings indicate novel mechanisms that modulate critical DNA retrotransposon activity, maintain chromosome conformation and contribute to central nervous system development.

ORGANISM(S): Mus musculus

PROVIDER: GSE247617 | GEO | 2024/06/01

REPOSITORIES: GEO

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Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (WGBS)

Project description:Short interspersed nuclear element (SINE) B2 are a type of DNA retrotransposon that organize three-dimensional genome during development. Containing binding sites for CCCTC-binding factor (CTCF), SINE_B2 serve as domain boundary elements that control chromatin state and initiate transcription of critical developmental genes. However, it is still unclear how SINE_B2 are regulated during neurodevelopment. Our findings indicate novel mechanisms that modulate critical DNA retrotransposon activity, maintain chromosome conformation and contribute to central nervous system development.

2024-06-01 | GSE247619 | GEO

Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (ChIP-Seq)

2024-06-01 | GSE247618 | GEO

B2 SINE expression during MHV68 infecton

Project description:Short interspersed nuclear elements (SINEs) are retrotransposons evolutionarily derived from endogenous RNA Polymerase III RNAs. Though SINE elements have undergone exaptation into gene regulatory elements, how transcribed SINE RNA impacts transcriptional and post-transcriptional regulation is largely unknown. This is partly due to a lack of information regarding which of the loci have transcriptional potential. Here, we present an approach (short interspersed nuclear element sequencing, SINE-seq), which selectively profiles RNA Polymerase III-derived SINE RNA, thereby identifying transcriptionally active SINE loci. Applying SINE-seq to monitor murine B2 SINE expression during a gammaherpesvirus infection revealed transcription from 28,270 SINE loci, with ~50% of active SINE elements residing within annotated RNA Polymerase II loci. Furthermore, B2 RNA can form intermolecular RNA-RNA interactions with complementary mRNAs, leading to nuclear retention of the targeted mRNA via a mechanism involving p54nrb. These findings illuminate a pathway for the selective regulation of mRNA export during stress via retrotransposon activation.

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Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells

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

2024-06-01 | GSE247620 | GEO

SINE RNAs trigger noncanonical NLRC4 inflammasome via DDX17

Project description:Short interspersed element (SINE) RNAs are upregulated by cellular stresses1 (heat shock, DNA damage and viral infection) and accumulate in human diseases (macular degeneration2, lupus3, and Alzheimer’s disease4). These transcripts activate inflammasomes5, a family of cytoplasmic multiprotein complexes that sense danger molecules and initiate innate immune responses by activating caspase-1-dependent cytokine production and inflammatory death6, but the molecular sensor of SINE RNAs is unknown. Here, we identify DDX17, a member of the DEAD box family of RNA helicases7, as a sensor of SINE RNAs requisite for inflammasome activation. Induction of caspase-1 cleavage and release of IL-1 and IL-18 by SINE RNAs requires dual recruitment of NLRP3 and NLRC4 but proceeds independent of NAIPs, immune sensors required for canonical NLRC4 activation by bacterial proteins8,9. Instead, SINE RNAs trigger DDX17–NLRC4 interaction, which licenses inflammasome activation. We also report increased levels of DDX17 protein and association of DDX17 and NLRC4 in the retinal pigmented epithelium (RPE) of human eyes with an advanced, untreatable form of age-related macular degeneration (AMD). Disrupting DDX17–NLRC4 signalling blocks SINE RNA-induced inflammasome activation in human RPE cells and RPE degeneration in an animal model of AMD. Our findings uncover a non-canonical mode of inflammasome activation by endogenous retrotransposon transcripts, and provide new potential targets for macular degeneration and potentially other diseases.

2022-06-09 | PXD016019 | Pride

Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells

Project description:Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells

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Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (WGBS)

Project description:Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (WGBS)

| PRJNA1039830 | ENA

Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (ChIP-Seq)

Project description:Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (ChIP-Seq)

| PRJNA1039826 | ENA

Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (Hi-C)

Project description:Histone methyltransferase SETDB1 silenced SINE B2 retrotransposons and maintained mitotic cell cycle of neural progenitor cells (Hi-C)

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RNA-seq analysis about Lx8-SINE B2 knocked down samples

Project description:We identified a novel long non-coding RNA Lx8-SINE B2, that is a marker of pluripotency. Depletion of Lx8-SINE B2 impacts embryonic stem cell self-renewal. RNA-seq analysis of Lx8-SINE B2 depletion revealed that a number of glycolytic genes with decreased expression. Mechanistically, we found that the Lx8-SINE B2 activates the glycolysis pathway by binding to Eno1. Collectively, our data suggest that Lx8-SINE B2 maintains the self-renewal of mESCs through glycolysis.

2022-09-19 | GSE182247 | GEO

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