ArticleScientific data2022
An atlas of endogenous DNA double-strand breaks arising during human neural cell fate determination.
Article in Scientific data, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Chromatin-associated intronic RNAs from long genes form introsomes that shape nuclear architecture in neuronal cells.bioRxiv : the preprint server for biology · 2026Article
- Somatic Mosaicism in Brain Disorders.Annual review of pathology · 2025Review
- Article
- Building the brain mosaic: an expanded view.Trends in genetics : TIG · 2024Review
- A Unifying Hypothesis for the Genome Dynamics Proposed to Underlie Neuropsychiatric Phenotypes.Genes · 2024Review
- Genomic origin, fragmentomics, and transcriptional properties of long cell-free DNA molecules in human plasma.Genome research · 2024Article
- An atlas of endogenous DNA double-strand breaks arising during human neural cell fate determination.Scientific data · 2022Article
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Endogenous DNA double-strand breaks (DSBs) occurring in neural cells have been implicated in the pathogenesis of neurodevelopmental disorders (NDDs). Currently, a genomic map of endogenous DSBs arising during human neurogenesis is missing. Here, we applied in-suspension Breaks Labeling In Situ and Sequencing (sBLISS), RNA-Seq, and Hi-C to chart the genomic landscape of DSBs and relate it to gene expression and genome architecture in 2D cultures of human neuroepithelial stem cells (NES), neural progenitor cells (NPC), and post-mitotic neural cells (NEU). Endogenous DSBs were enriched at the promoter and along the gene body of transcriptionally active genes, at the borders of topologically associating domains (TADs), and around chromatin loop anchors. NDD risk genes harbored significantly more DSBs in comparison to other protein-coding genes, especially in NEU cells. We provide sBLISS, RNA-Seq, and Hi-C datasets for each differentiation stage, and all the scripts needed to reproduce our analyses. Our datasets and tools represent a unique resource that can be harnessed to investigate the role of genome fragility in the pathogenesis of NDDs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.