ArticleBrain : a journal of neurology2023
Speech- and language-linked FOXP2 mutation targets protein motors in striatal neurons.
Article in Brain : a journal of neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Molecular and cell type-specific determinants of inferior colliculus development and auditory function.bioRxiv : the preprint server for biology · 2026Article
- Activity-dependent development of vocal circuits in the neonatal rodent forebrain.EMBO reports · 2026Article
- Neuroprotective Effects of Cerium Oxide Nanoparticles During Spaceflight.Small science · 2026Article
- The effect of human-specific genetic variants on neuronal spinogenesis.Frontiers in genetics · 2026Review
- FOXP2-Dependent Vulnerability of RGCs Under Acute Ocular Hypertension.Molecular neurobiology · 2025Article
- Tubular FoxP2 and Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2025Article
- Compensation between FOXP transcription factors maintains proper striatal function.Cell reports · 2024Article
- Modelling TDP-43 proteinopathy in Drosophila uncovers shared and neuron-specific targets across ALS and FTD relevant circuits.Acta neuropathologica communications · 2023Article
- Compensation between FOXP transcription factors maintains proper striatal function.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Human speech and language are among the most complex motor and cognitive abilities. The discovery of a mutation in the transcription factor FOXP2 in KE family members with speech disturbances has been a landmark example of the genetic control of vocal communication in humans. Cellular mechanisms underlying this control have remained unclear. By leveraging FOXP2 mutation/deletion mouse models, we found that the KE family FOXP2R553H mutation directly disables intracellular dynein-dynactin 'protein motors' in the striatum by induction of a disruptive high level of dynactin1 that impairs TrkB endosome trafficking, microtubule dynamics, dendritic outgrowth and electrophysiological activity in striatal neurons alongside vocalization deficits. Dynactin1 knockdown in mice carrying FOXP2R553H mutations rescued these cellular abnormalities and improved vocalization. We suggest that FOXP2 controls vocal circuit formation by regulating protein motor homeostasis in striatal neurons, and that its disruption could contribute to the pathophysiology of FOXP2 mutation/deletion-associated speech disorders.
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Registered trials
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