ArticleScientific reports2020
CDCA7 and HELLS suppress DNA:RNA hybrid-associated DNA damage at pericentromeric repeats.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- CDCA7 targets LSH to DNA maintenance methylation in S phase and transcription regulation in interphase via two distinct DNA-binding modes.Nucleic acids research · 2026Article
- Structure of human lymphoid-specific helicase HELLS in its autoinhibited state.Nucleic acids research · 2026Article
- SFPQ directs histone H3.3 deposition to R-loops in DNA repeats to protect genome stability.Nature communications · 2026Article
- Missense substitutions in the BTB domain of ZBTB24 can lead to protein instability and cause ICF2 syndrome.Human molecular genetics · 2026Article
- Transcriptional PBR cycles at pericentromeric repeats cause gross chromosomal rearrangements through Rad52-dependent ADR-loop formation.Nucleic acids research · 2026Article
- Structure of human lymphoid-specific helicase HELLS in its autoinhibitory state.bioRxiv : the preprint server for biology · 2025Article
- Antibiotics induce overexpression of alpha satellite DNA accompanied with epigenetic changes at alpha satellite arrays as well as genome-wide.Epigenetics & chromatin · 2025Article
- ZBTB24 is a conserved multifaceted transcription factor at genes and centromeres that governs the DNA methylation state and expression of satellite repeats.Human molecular genetics · 2025Article
- CDCA7 is an evolutionarily conserved hemimethylated DNA sensor in eukaryotes.Science advances · 2024Article
- HELLS regulates transcription in T-cell lymphomas by reducing unscheduled R-loops and by facilitating RNAPII progression.Nucleic acids research · 2024Article
- Exploring the intersection of epigenetics, DNA repair, and immunology from studies of ICF syndrome, an inborn error of immunity.Frontiers in immunology · 2024Review
- A novel iPSC-based model of ICF syndrome subtype 2 recapitulates the molecular phenotype of ZBTB24 deficiency.Frontiers in immunology · 2024Article
- Gross Chromosomal Rearrangement at Centromeres.Biomolecules · 2023Review
- Alpha Satellite DNA in Targeted Drug Therapy for Prostate Cancer.International journal of molecular sciences · 2023Article
- Coevolution of the CDCA7-HELLS ICF-related nucleosome remodeling complex and DNA methyltransferases.eLife · 2023Article
- Germinal center output is sustained by HELLS-dependent DNA-methylation-maintenance in B cells.Nature communications · 2023Article
- Coevolution of the CDCA7-HELLS ICF-related nucleosome remodeling complex and DNA methyltransferases.bioRxiv : the preprint server for biology · 2023Article
- DDM1-mediated R-loop resolution and H2A.Z exclusion facilitates heterochromatin formation in Arabidopsis.Science advances · 2023Article
- Seminars in cell and development biology on histone variants remodelers of H2A variants associated with heterochromatin.Seminars in cell & developmental biology · 2023Review
- Regulatory mechanism and biological function of UHRF1-DNMT1-mediated DNA methylation.Functional & integrative genomics · 2022Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunodeficiency, centromeric instability, facial anomalies (ICF) syndrome is a rare autosomal recessive disorder that is caused by mutations in either DNMT3B, ZBTB24, CDCA7, HELLS, or yet unidentified gene(s). Previously, we reported that the CDCA7/HELLS chromatin remodeling complex facilitates non-homologous end-joining. Here, we show that the same complex is required for the accumulation of proteins on nascent DNA, including the DNMT1/UHRF1 maintenance DNA methylation complex as well as proteins involved in the resolution or prevention of R-loops composed of DNA:RNA hybrids and ssDNA. Consistent with the hypomethylation state of pericentromeric repeats, the transcription and formation of aberrant DNA:RNA hybrids at the repeats were increased in ICF mutant cells. Furthermore, the ectopic expression of RNASEH1 reduced the accumulation of DNA damage at a broad range of genomic regions including pericentromeric repeats in these cells. Hence, we propose that hypomethylation due to inefficient DNMT1/UHRF1 recruitment at pericentromeric repeats by defects in the CDCA7/HELLS complex could induce pericentromeric instability, which may explain a part of the molecular pathogenesis of ICF syndrome.
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