ArticlePLoS biology2024
Loss of Katnal2 leads to ependymal ciliary hyperfunction and autism-related phenotypes in mice.
Article in PLoS biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Article
- First Reported Co-Occurrence of Bardet-Biedl Syndrome Type 10 and Autism Spectrum Disorder: A Case Report and Clinical Review.Molecular syndromology · 2026Article
- Fecal microbiota transplantation and Akkermansia muciniphila restore neurodevelopment and behavior via the gut-brain axis in autism-like zebrafish.The ISME journal · 2026Article
- Fingolimod Exerts Therapeutic Effects on Autistic Mice via Improving the Structure and Function of Meningeal Lymphatics.CNS neuroscience & therapeutics · 2025Article
- Multiciliated ependymal cells: an update on biology and pathology in the adult brain.Acta neuropathologica · 2024Review
- KATNAL2 mutations link ciliary dysfunction to hydrocephalus and autism.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
23 authors.
Funding
Abstract
Autism spectrum disorders (ASD) frequently accompany macrocephaly, which often involves hydrocephalic enlargement of brain ventricles. Katnal2 is a microtubule-regulatory protein strongly linked to ASD, but it remains unclear whether Katnal2 knockout (KO) in mice leads to microtubule- and ASD-related molecular, synaptic, brain, and behavioral phenotypes. We found that Katnal2-KO mice display ASD-like social communication deficits and age-dependent progressive ventricular enlargements. The latter involves increased length and beating frequency of motile cilia on ependymal cells lining ventricles. Katnal2-KO hippocampal neurons surrounded by enlarged lateral ventricles show progressive synaptic deficits that correlate with ASD-like transcriptomic changes involving synaptic gene down-regulation. Importantly, early postnatal Katnal2 re-expression prevents ciliary, ventricular, and behavioral phenotypes in Katnal2-KO adults, suggesting a causal relationship and a potential treatment. Therefore, Katnal2 negatively regulates ependymal ciliary function and its deletion in mice leads to ependymal ciliary hyperfunction and hydrocephalus accompanying ASD-related behavioral, synaptic, and transcriptomic changes.
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Registered trials
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