ArticleNucleic acids research2022
CHD8 suppression impacts on histone H3 lysine 36 trimethylation and alters RNA alternative splicing.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- CHD8-Dependent Chromatin Licensing Sustains Trophoblast Stem Cell Transcriptional Programs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Genome-wide associations of structural variants with human traits through imputation from long-read assemblies.Nature genetics · 2026Article
- Molecular interactions of Chd8 in mouse brain highlights a role in chromatin-associated RNA processing.bioRxiv : the preprint server for biology · 2025Article
- Persistent cortical excitatory neuron dysregulation in adultResearch square · 2025Article
- Elucidating neuroepigenetic mechanisms to inform targeted therapeutics for brain disorders.iScience · 2025Review
- SINEUP RNA rescues molecular phenotypes associated with CHD8 suppression in autism spectrum disorder model systems.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Identification of Therapeutic Targets in Autism Spectrum Disorder through CHD8-Notch Pathway Interaction Analysis.PloS one · 2025Article
- Key gene screening and diagnostic model establishment for acute type a aortic dissection.Frontiers in genetics · 2025Article
- Article
- Identification and experimental validation of common genes associated with both pulmonary arterial hypertension and major depressive disorder.Frontiers in psychiatry · 2025Article
- The crosstalk between alternative splicing and circular RNA in cancer: pathogenic insights and therapeutic implications.Cellular & molecular biology letters · 2024Review
- Autism-associated CHD8 controls reactive gliosis and neuroinflammation via remodeling chromatin in astrocytes.Cell reports · 2024Article
- Neurodevelopmental functions of CHD8: new insights and questions.Biochemical Society transactions · 2024Review
- Whole genome methylation sequencing in blood identifies extensive differential DNA methylation in late-onset dementia due to Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Epigenetic Causes of Overgrowth Syndromes.The Journal of clinical endocrinology and metabolism · 2024Review
- Heterozygous deletion of the autism-associated gene CHD8 impairs synaptic function through widespread changes in gene expression and chromatin compaction.American journal of human genetics · 2023Article
- From X-inactivation to neurodevelopment: CHD8-transcription factors (TFs) competitive binding at regulatory regions of CHD8 target genes can contribute to correct neuronal differentiation.Current research in neurobiology · 2023Review
- Age-differential sexual dimorphisms in CHD8-S62X-mutant mouse synapses and transcriptomes.Frontiers in molecular neuroscience · 2023Article
Corrections and comments
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Authors and funding
21 authors at 7 institutions in 4 countries.
Funding
Abstract
Disruptive mutations in the chromodomain helicase DNA-binding protein 8 gene (CHD8) have been recurrently associated with autism spectrum disorders (ASDs). Here we investigated how chromatin reacts to CHD8 suppression by analyzing a panel of histone modifications in induced pluripotent stem cell-derived neural progenitors. CHD8 suppression led to significant reduction (47.82%) in histone H3K36me3 peaks at gene bodies, particularly impacting on transcriptional elongation chromatin states. H3K36me3 reduction specifically affects highly expressed, CHD8-bound genes and correlates with altered alternative splicing patterns of 462 genes implicated in 'regulation of RNA splicing' and 'mRNA catabolic process'. Mass spectrometry analysis uncovered a novel interaction between CHD8 and the splicing regulator heterogeneous nuclear ribonucleoprotein L (hnRNPL), providing the first mechanistic insights to explain the CHD8 suppression-derived splicing phenotype, partly implicating SETD2, a H3K36me3 methyltransferase. In summary, our results point toward broad molecular consequences of CHD8 suppression, entailing altered histone deposition/maintenance and RNA processing regulation as important regulatory processes in ASD.
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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.