Abstract
Development of proficient spoken language skills is disrupted by mutations of the FOXP2 transcription factor. A heterozygous missense mutation in the KE family causes speech apraxia, involving difficulty producing words with complex learned sequences of syllables. Manipulations in songbirds have helped to elucidate the role of this gene in vocal learning, but findings in non-human mammals have been limited or inconclusive. Here, we performed a systematic study of ultrasonic vocalizations (USVs) of adult male mice carrying the KE family mutation. Using novel statistical tools, we found that Foxp2 heterozygous mice did not have detectable changes in USV syllable acoustic structure, but produced shorter sequences and did not shift to more complex syntax in social contexts where wildtype animals did. Heterozygous mice also displayed a shift in the position of their rudimentary laryngeal motor cortex (LMC) layer-5 neurons. Our findings indicate that although mouse USVs are mostly innate, the underlying contributions of FoxP2 to sequencing of vocalizations are conserved with humans.
Highlights
Spoken language plays a central role in our culture and society, which we use to express emotions, convey ideas, and communicate
Since the Foxp2-R552H mutation was backcrossed on a different wildtype background (C57BL6/J, hereafter called C57) than the strain used for our previous study (B6D2F1/J, hereafter called B6; Chabout et al, 2015), we first checked whether the C57 wildtype showed social context differences
In female-associated contexts (UF, live female condition (LF), and anesthetized female condition (AF)), Foxp2 heterozygotes had a nonsignificant trend for lower syllable production rates (Figure 2A), which was related to an interaction with sequence length, described later in this study
Summary
Spoken language plays a central role in our culture and society, which we use to express emotions, convey ideas, and communicate. We belong to one of few species that learn to produce new vocalizations These vocal behaviors are susceptible to a range of impairments, making dramatic impacts on our everyday life. Such deficits represent a major public health issue, with the prevalence of speech-sound disorder in young children estimated at 8–9% (NIDCD, 2010). Affected individuals have difficulties mastering the coordinated movement sequences of syllables/phonemes for fluent speech, described as developmental verbal dyspraxia (DVD) or childhood apraxia of speech (CAS), as well as impacting written language.
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