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Endogenous retroviruses direct the evolution of lineage-specific imprinting

ABSTRACT: Endogenous retroviruses direct the evolution of lineage-specific imprinting

PROVIDER: PRJNA521704 | ENA |

REPOSITORIES: ENA

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Endogenous retroviruses direct the evolution of lineage-specific imprinting

Project description:Imprinted genes are expressed from a single parental allele. In mammals, this unusual mode of transcription generally depends on the epigenetic silencing of the other allele by DNA methylation (DNAme) established in the germline. While many species-specific imprinted orthologues have been documented in eutherians, the molecular mechanisms underlying the evolutionary switch from biallelic to imprinted expression are currently unknown. During mouse oogenesis, gametic differentially methylated regions (gDMRs) acquire DNAme in a process guided by transcription. Here we show that transcription initiating in proximal lineage-specific endogenous retroviruses (ERVs) is likely responsible for DNAme established in oocytes at 4/7 mouse-specific and 22/155 human-specific maternal gDMRs. The latter can be further divided into Catarrhini (old-world monkeys and apes)- or Hominoidea (ape)-specific gDMRs, which are embedded within transcription units initiating in ERVs specific to these primate lineages. Using CRISPR-Cas9 mutagenesis, we deleted the relevant murine-specific ERVs upstream of the maternally methylated genes Impact and Slc38a4. Strikingly, imprinting was lost in the offspring of dams harboring these deletions and biallelic expression was observed, revealing a novel evolutionary mechanism by which maternally silenced genes arise from biallelically expressed progenitors.

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Hijacking of transcriptional condensates by endogenous retroviruses

Project description:Hijacking of transcriptional condensates by endogenous retroviruses

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Endogenous retroviruses promote prion-like spreading of proteopathic seeds

Project description:Prion-like spreading of protein misfolding is characteristic for neurodegenerative diseases, but the exact mechanisms of intercellular protein aggregate dissemination remain unresolved. Evidence accumulates that endogenous retroviruses, remnants of viral germline infections that are normally epigenetically silenced, become upregulated in neurodegenerative diseases such as amyotrophic lateral sclerosis and tauopathies. Here we uncover that activation of endogenous retroviruses affects prion-like spreading of proteopathic seeds. To identify changes in the proteome of donor cells that might contribute to protein aggregate spreading, we performed mass spectrometry analyses of total cell lysates and donor EV fractions using N2a cells expressing HA epitope-tagged Sup35 NM prion protein at early (P07) and late passages (P16) post cryopreservation. Among the proteins increased in donor cells and EVs upon prolonged culture, we identified mouse endogenous MLV retrovirus proteins to be highly increased.

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H3.3 deposition at endogenous retroviruses in embryonic stem cells

Project description:We report DAXX-dependent deposition of histone H3.3 at at endogenous retroviruses in embryonic stem cells.

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TRIM28 silences endogenous retroviruses in neural progenitor cells

Project description:Here we show that in neural progenitor cells (NPCs) TRIM28 silences transcription of two groups of endogenous retroviruses (ERVs): IAP1 and MMERVK10C. Derepression of ERVs in Trim28-deficient NPCs was associated with a loss of H3K9me3 and resulted in transcriptional upregulation and reverse transcription. These findings demonstrate a unique dynamic transcriptional regulation of ERVs in NPCs. Analysis of upregulation of ERVs in Trim28-deficient NPCs

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Activation of endogenous retroviruses during brain development causes neuroinflammation

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