Autism and speech and language deficits are predominantly found in boys, however the causative mechanisms for this sex bias are unknown. Human FOXP1 is associated with autism, intellectual disability and speech and language deficits. Its closely related family member FOXP2 is involved in speech and language disorder and Foxp2 deficient mice have demonstrated an absence of ultrasonic vocalizations. Since Foxp1 and Foxp2 form heterodimers for transcriptional regulation, we investigated ultrasonic vocalization (USV) in neonatal brain-specific Foxp1 KO mice. Foxp1 KO pups had strongly reduced USV and lacked the sex-specific call rate from WT pups, indicating that Foxp1 is essential for normal USV. As expression differences of Foxp1 or Foxp2 could explain the sex-dimorphic vocalization in WT animals, we quantified both proteins in the striatum and cortex at P7.5 and detected a sex-specific expression of Foxp2 in the striatum. We further analyzed Foxp1 and Foxp2 expression in the striatum and cortex of CD1 mice at different embryonic and postnatal stages and observed sex differences in both genes at E17.5 and P7.5.

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