A Foxp2 mutation implicated in human speech deficits alters sequencing of ultrasonic vocalizations in adult male mice
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 hel...
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2016-10-01
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Online Access: | http://journal.frontiersin.org/Journal/10.3389/fnbeh.2016.00197/full |
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doaj-87588436d85e4c2b891e53d890a9f42c2020-11-24T22:56:06ZengFrontiers Media S.A.Frontiers in Behavioral Neuroscience1662-51532016-10-011010.3389/fnbeh.2016.00197214111A Foxp2 mutation implicated in human speech deficits alters sequencing of ultrasonic vocalizations in adult male miceJonathan Chabout0Jonathan Chabout1Abhra Sarkar2Sheel R Patel3Taylor Radden4David B Dunson5Simon E Fisher6Simon E Fisher7Erich D Jarvis8Erich D Jarvis9Erich D Jarvis10Duke University Medical CenterHoward Hughes Medical InstituteDuke UniversityDuke University Medical CenterDuke University Medical CenterDuke UniversityMax Planck Institute for PsycholinguisticsRadboud UniversityDuke University Medical CenterHoward Hughes Medical InstituteThe Rockefeller UniversityDevelopment 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 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.http://journal.frontiersin.org/Journal/10.3389/fnbeh.2016.00197/fullsyntaxFoxP2KE familysongultrasonic vocalizationsSpeech apraxia |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jonathan Chabout Jonathan Chabout Abhra Sarkar Sheel R Patel Taylor Radden David B Dunson Simon E Fisher Simon E Fisher Erich D Jarvis Erich D Jarvis Erich D Jarvis |
spellingShingle |
Jonathan Chabout Jonathan Chabout Abhra Sarkar Sheel R Patel Taylor Radden David B Dunson Simon E Fisher Simon E Fisher Erich D Jarvis Erich D Jarvis Erich D Jarvis A Foxp2 mutation implicated in human speech deficits alters sequencing of ultrasonic vocalizations in adult male mice Frontiers in Behavioral Neuroscience syntax FoxP2 KE family song ultrasonic vocalizations Speech apraxia |
author_facet |
Jonathan Chabout Jonathan Chabout Abhra Sarkar Sheel R Patel Taylor Radden David B Dunson Simon E Fisher Simon E Fisher Erich D Jarvis Erich D Jarvis Erich D Jarvis |
author_sort |
Jonathan Chabout |
title |
A Foxp2 mutation implicated in human speech deficits alters sequencing of ultrasonic vocalizations in adult male mice |
title_short |
A Foxp2 mutation implicated in human speech deficits alters sequencing of ultrasonic vocalizations in adult male mice |
title_full |
A Foxp2 mutation implicated in human speech deficits alters sequencing of ultrasonic vocalizations in adult male mice |
title_fullStr |
A Foxp2 mutation implicated in human speech deficits alters sequencing of ultrasonic vocalizations in adult male mice |
title_full_unstemmed |
A Foxp2 mutation implicated in human speech deficits alters sequencing of ultrasonic vocalizations in adult male mice |
title_sort |
foxp2 mutation implicated in human speech deficits alters sequencing of ultrasonic vocalizations in adult male mice |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Behavioral Neuroscience |
issn |
1662-5153 |
publishDate |
2016-10-01 |
description |
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 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. |
topic |
syntax FoxP2 KE family song ultrasonic vocalizations Speech apraxia |
url |
http://journal.frontiersin.org/Journal/10.3389/fnbeh.2016.00197/full |
work_keys_str_mv |
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