ArticleScientific reports2020
Region-specific Foxp2 deletions in cortex, striatum or cerebellum cannot explain vocalization deficits observed in spontaneous global knockouts.
Article in Scientific reports, 2020. 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, 39 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
- A Gene-Expression Based Comparison of Murine and Human Inhibitory Interneurons in the Cerebellar Cortex and Nuclei.Cerebellum (London, England) · 2025Article
- Rodent ultrasonic vocal interaction resolved with millimeter precision using hybrid beamforming.eLife · 2023Article
- Mafa-dependent GABAergic activity promotes mouse neonatal apneas.Nature communications · 2022Article
- A Model of Discovery: The Role of Imaging Established and Emerging Non-mammalian Models in Neuroscience.Frontiers in molecular neuroscience · 2022Review
- Molecular networks of the FOXP2 transcription factor in the brain.EMBO reports · 2021Review
- MET Receptor Tyrosine Kinase Regulates Lifespan Ultrasonic Vocalization and Vagal Motor Neuron Development.Frontiers in neuroscience · 2021Article
- Subtle alterations in neonatal neurodevelopment following early or late exposure to prenatal maternal immune activation in mice.NeuroImage. Clinical · 2021Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
FOXP2 has been identified as a gene related to speech in humans, based on rare mutations that yield significant impairments in speech at the level of both motor performance and language comprehension. Disruptions of the murine orthologue Foxp2 in mouse pups have been shown to interfere with production of ultrasonic vocalizations (USVs). However, it remains unclear which structures are responsible for these deficits. Here, we show that conditional knockout mice with selective Foxp2 deletions targeting the cerebral cortex, striatum or cerebellum, three key sites of motor control with robust neural gene expression, do not recapture the profile of pup USV deficits observed in mice with global disruptions of this gene. Moreover, we observed that global Foxp2 knockout pups show substantive reductions in USV production as well as an overproduction of short broadband noise "clicks", which was not present in the brain region-specific knockouts. These data indicate that deficits of Foxp2 expression in the cortex, striatum or cerebellum cannot solely explain the disrupted vocalization behaviours in global Foxp2 knockouts. Our findings raise the possibility that the impact of Foxp2 disruption on USV is mediated at least in part by effects of this gene on the anatomical prerequisites for vocalizing.
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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.