ArticleBiology open2022
Autism-associated CHD8 keeps proliferation of human neural progenitors in check by lengthening the G1 phase of the cell cycle.
Article in Biology open, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- MELK is Required for G2/M Phase Progression in Cortical Progenitors: Insights from Rare ASD-Associated Variants.Cellular and molecular neurobiology · 2026Article
- Article
- BRD1 haploinsufficiency alters early neuronal programming and disrupts maturation in human induced glutamatergic neurons.Research square · 2026Article
- Defective Neural Stem and Progenitor Cell Proliferation in Neurodevelopmental Disorders.Journal of developmental biology · 2025Review
- A CHD8-TRRAP axis facilitates MYC and E2F target gene regulation in human neural stem cells.iScience · 2025Article
- Identification and experimental validation of common genes associated with both pulmonary arterial hypertension and major depressive disorder.Frontiers in psychiatry · 2025Article
- Age-differential sexual dimorphisms in CHD8-S62X-mutant mouse synapses and transcriptomes.Frontiers in molecular neuroscience · 2023Article
- Developmental pyrethroid exposure and age influence phenotypes in a Chd8 haploinsufficient autism mouse model.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
De novo mutations (DNMs) in chromodomain helicase DNA binding protein 8 (CHD8) are associated with a specific subtype of autism characterized by enlarged heads and distinct cranial features. The vast majority of these DNMs are heterozygous loss-of-function mutations with high penetrance for autism. CHD8 is a chromatin remodeler that preferentially regulates expression of genes implicated in early development of the cerebral cortex. How CHD8 haploinsufficiency alters the normal developmental trajectory of the brain is poorly understood and debated. Using long-term single-cell imaging, we show that disruption of a single copy of CHD8 in human neural precursor cells (NPCs) markedly shortens the G1 phase of the cell cycle. Consistent with faster progression of CHD8+/- NPCs through G1 and the G1/S checkpoint, we observed increased expression of E cyclins and elevated phosphorylation of Erk in these mutant cells - two central signaling pathways involved in S phase entry. Thus, CHD8 keeps proliferation of NPCs in check by lengthening G1, and mono-allelic disruption of this gene alters cell-cycle timing in a way that favors self-renewing over neurogenic cell divisions. Our findings further predict enlargement of the neural progenitor pool in CHD8+/- developing brains, providing a mechanistic basis for macrocephaly in this autism subtype.
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Registered trials
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