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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.

Region-specific Foxp2 deletions in cortex, striatum or cerebellum cannot explain vocalization deficits observed in spontaneous global knockouts