ArticleDevelopment (Cambridge, England)2023
Pleiotropy of autism-associated chromatin regulators.
Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Autism and Neurodegeneration: Distinct Disorders or a Shared Biological Continuum?Brain sciences · 2026Review
- Disruption of DNA Repair as an Emerging Epigenetic Mechanism Underlying Autism Spectrum Disorder.Current psychiatry reports · 2026Review
- Pharmaco-behavioral profiling identifies suppressors of autism gene-associated phenotypes in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Novel mouse line with D277N mutation in theFrontiers in cell and developmental biology · 2026Article
- KMT5B in Cancerous and Noncancerous Diseases: Clinical and Mechanical Considerations.International journal of medical sciences · 2026Review
- LncRNA CISTR-ACT regulates cell size in human and mouse by guiding FOSL2.Nature communications · 2025Article
- Molecular interactions of Chd8 in mouse brain highlights a role in chromatin-associated RNA processing.bioRxiv : the preprint server for biology · 2025Article
- Multiple autism genes influence GABA neuron remodeling via distinct developmental trajectories.Genetics · 2025Article
- Contribution of rare coding variants to microcephaly in individuals with neurodevelopmental disorders.Genome medicine · 2025Article
- Functional Neurogenomics to Dissect Disease Mechanisms Across Models.Annual review of genomics and human genetics · 2025Review
- Multiple autism genes influence GABA neuron remodeling via distinct developmental trajectories.bioRxiv : the preprint server for biology · 2025Article
- Ciliary biology intersects autism and congenital heart disease.Development (Cambridge, England) · 2025Article
- Disrupted diencephalon development and neuropeptidergic pathways in zebrafish with autism-risk mutations.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Autism gene variants disrupt enteric neuron migration and cause gastrointestinal dysmotility.Nature communications · 2025Article
- Convergence of autism proteins at the cilium.bioRxiv : the preprint server for biology · 2025Article
- Molecular and network disruptions in neurodevelopment uncovered by single cell transcriptomics analysis ofHeliyon · 2024Article
- Neurodevelopmental functions of CHD8: new insights and questions.Biochemical Society transactions · 2024Review
- Neuroplasticity of children in autism spectrum disorder.Frontiers in psychiatry · 2024Review
- A roadmap to cure CHD2-related disorders.Therapeutic advances in rare diseaseReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 1 institution in 1 country.
Funding
Abstract
Gene ontology analyses of high-confidence autism spectrum disorder (ASD) risk genes highlight chromatin regulation and synaptic function as major contributors to pathobiology. Our recent functional work in vivo has additionally implicated tubulin biology and cellular proliferation. As many chromatin regulators, including the ASD risk genes ADNP and CHD3, are known to directly regulate both tubulins and histones, we studied the five chromatin regulators most strongly associated with ASD (ADNP, CHD8, CHD2, POGZ and KMT5B) specifically with respect to tubulin biology. We observe that all five localize to microtubules of the mitotic spindle in vitro in human cells and in vivo in Xenopus. Investigation of CHD2 provides evidence that mutations present in individuals with ASD cause a range of microtubule-related phenotypes, including disrupted localization of the protein at mitotic spindles, cell cycle stalling, DNA damage and cell death. Lastly, we observe that ASD genetic risk is significantly enriched among tubulin-associated proteins, suggesting broader relevance. Together, these results provide additional evidence that the role of tubulin biology and cellular proliferation in ASD warrants further investigation and highlight the pitfalls of relying solely on annotated gene functions in the search for pathological mechanisms.
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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.