ArticleNature communications2024
DNA methylation governs the sensitivity of repeats to restriction by the HUSH-MORC2 corepressor.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Silencing the genome: role of HUSH complex in retrotransposon regulation and cancer development.Medical oncology (Northwood, London, England) · 2026Review
- LINE-1 Epigenetic Repression and Regulation of Immunity.Viruses · 2026Review
- Review
- Fiber-TEnCATS reveals haplotype-specific chromatin accessibility and DNA methylation at human L1HS loci.bioRxiv : the preprint server for biology · 2026Article
- Review
- Article
- Review
- Loss of SETDB1-mediated H3K9me3 in human neural progenitor cells leads to transcriptional activation of L1 retrotransposons.Nucleic acids research · 2026Article
- Antagonistic regulation of LINE-1/Alu elements and their repressor APOBEC3B in cellular senescence.Mobile DNA · 2025Article
- LINE-1 retrotransposons mediate cis-acting transcriptional control in human pluripotent stem cells and regulate early brain development.Cell genomics · 2025Article
- Identification and characterization of a human MORC2 DNA binding region that is required for gene silencing.Nucleic acids research · 2025Article
- Biological functions and molecular mechanisms of MORC2 in human diseases.Molecules and cells · 2025Review
- TASOR expression in naive embryonic stem cells safeguards their developmental potential.Cell reports · 2024Article
- PRC1.6 localizes on chromatin with the human silencing hub (HUSH) complex for promoter-specific silencing.bioRxiv : the preprint server for biology · 2024Article
- Identification and characterization of a human MORC2 DNA binding region that is required for gene silencing.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
17 authors.
Funding
Abstract
The human silencing hub (HUSH) complex binds to transcripts of LINE-1 retrotransposons (L1s) and other genomic repeats, recruiting MORC2 and other effectors to remodel chromatin. How HUSH and MORC2 operate alongside DNA methylation, a central epigenetic regulator of repeat transcription, remains largely unknown. Here we interrogate this relationship in human neural progenitor cells (hNPCs), a somatic model of brain development that tolerates removal of DNA methyltransferase DNMT1. Upon loss of MORC2 or HUSH subunit TASOR in hNPCs, L1s remain silenced by robust promoter methylation. However, genome demethylation and activation of evolutionarily-young L1s attracts MORC2 binding, and simultaneous depletion of DNMT1 and MORC2 causes massive accumulation of L1 transcripts. We identify the same mechanistic hierarchy at pericentromeric α-satellites and clustered protocadherin genes, repetitive elements important for chromosome structure and neurodevelopment respectively. Our data delineate the epigenetic control of repeats in somatic cells, with implications for understanding the vital functions of HUSH-MORC2 in hypomethylated contexts throughout human development.
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