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Williams Syndrome, Human Self-Domestication, and Language Evolution

Language evolution resulted from changes in our biology, behavior, and culture. One source of these changes might be human self-domestication. Williams syndrome (WS) is a clinical condition with a clearly defined genetic basis which results in a distinctive behavioral and cognitive profile, includin...

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Detalles Bibliográficos
Autores principales: Niego, Amy, Benítez-Burraco, Antonio
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6431629/
https://www.ncbi.nlm.nih.gov/pubmed/30936846
http://dx.doi.org/10.3389/fpsyg.2019.00521
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author Niego, Amy
Benítez-Burraco, Antonio
author_facet Niego, Amy
Benítez-Burraco, Antonio
author_sort Niego, Amy
collection PubMed
description Language evolution resulted from changes in our biology, behavior, and culture. One source of these changes might be human self-domestication. Williams syndrome (WS) is a clinical condition with a clearly defined genetic basis which results in a distinctive behavioral and cognitive profile, including enhanced sociability. In this paper we show evidence that the WS phenotype can be satisfactorily construed as a hyper-domesticated human phenotype, plausibly resulting from the effect of the WS hemideletion on selected candidates for domestication and neural crest (NC) function. Specifically, we show that genes involved in animal domestication and NC development and function are significantly dysregulated in the blood of subjects with WS. We also discuss the consequences of this link between domestication and WS for our current understanding of language evolution.
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spelling pubmed-64316292019-04-01 Williams Syndrome, Human Self-Domestication, and Language Evolution Niego, Amy Benítez-Burraco, Antonio Front Psychol Psychology Language evolution resulted from changes in our biology, behavior, and culture. One source of these changes might be human self-domestication. Williams syndrome (WS) is a clinical condition with a clearly defined genetic basis which results in a distinctive behavioral and cognitive profile, including enhanced sociability. In this paper we show evidence that the WS phenotype can be satisfactorily construed as a hyper-domesticated human phenotype, plausibly resulting from the effect of the WS hemideletion on selected candidates for domestication and neural crest (NC) function. Specifically, we show that genes involved in animal domestication and NC development and function are significantly dysregulated in the blood of subjects with WS. We also discuss the consequences of this link between domestication and WS for our current understanding of language evolution. Frontiers Media S.A. 2019-03-18 /pmc/articles/PMC6431629/ /pubmed/30936846 http://dx.doi.org/10.3389/fpsyg.2019.00521 Text en Copyright © 2019 Niego and Benítez-Burraco. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Psychology
Niego, Amy
Benítez-Burraco, Antonio
Williams Syndrome, Human Self-Domestication, and Language Evolution
title Williams Syndrome, Human Self-Domestication, and Language Evolution
title_full Williams Syndrome, Human Self-Domestication, and Language Evolution
title_fullStr Williams Syndrome, Human Self-Domestication, and Language Evolution
title_full_unstemmed Williams Syndrome, Human Self-Domestication, and Language Evolution
title_short Williams Syndrome, Human Self-Domestication, and Language Evolution
title_sort williams syndrome, human self-domestication, and language evolution
topic Psychology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6431629/
https://www.ncbi.nlm.nih.gov/pubmed/30936846
http://dx.doi.org/10.3389/fpsyg.2019.00521
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