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Bapx1 upregulation is associated with ectopic mandibular cartilage development in amphibians

BACKGROUND: The emergence of novel structures during evolution is crucial for creating variation among organisms, but the underlying processes which lead to the emergence of evolutionary novelties are poorly understood. The gnathostome jaw joint is such a novelty, and the incorporation of bapx1 expr...

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Autores principales: Lukas, Paul, Olsson, Lennart
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5998585/
https://www.ncbi.nlm.nih.gov/pubmed/29942645
http://dx.doi.org/10.1186/s40851-018-0101-3
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author Lukas, Paul
Olsson, Lennart
author_facet Lukas, Paul
Olsson, Lennart
author_sort Lukas, Paul
collection PubMed
description BACKGROUND: The emergence of novel structures during evolution is crucial for creating variation among organisms, but the underlying processes which lead to the emergence of evolutionary novelties are poorly understood. The gnathostome jaw joint is such a novelty, and the incorporation of bapx1 expression into the intermediate first pharyngeal arch may have played a major role in the evolution of this joint. Knockdown experiments revealed that loss of bapx1 function leads to the loss of the jaw joint, because Meckel’s cartilage and the palatoquadrate fuse during development. We used Xenopus laevis and Ambystoma mexicanum to further investigate the function of bapx1 in amphibians. Bapx1 expression levels were upregulated through the use of Ly-294,002 and we investigated the potential consequences of the enhanced bapx1 expression in amphibians to test the hypothesized joint inducing function of bapx1. RESULTS: We show that Ly-294,002 upregulates bapx1 expression in vivo. Additionally, ectopic mandibular arch derived cartilages develop after Ly-294,002 treatment. These ectopic cartilages are dorsoventrally oriented rods situated lateral to the palatoquadrate. The development of these additional cartilages did not change the muscular arrangement of mandibular arch-derived muscles. CONCLUSIONS: Development of additional mandibular cartilages is not unusual in larval anurans. Therefore, changes in the bapx1 expression during evolution may have been the reason for the development of several additional cartilages in the larval anuran jaw. Furthermore, our observations imply a joint-promoting function of bapx1, which further substantiates its hypothetical role in the evolution of the gnathostome jaw joint.
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spelling pubmed-59985852018-06-25 Bapx1 upregulation is associated with ectopic mandibular cartilage development in amphibians Lukas, Paul Olsson, Lennart Zoological Lett Research Article BACKGROUND: The emergence of novel structures during evolution is crucial for creating variation among organisms, but the underlying processes which lead to the emergence of evolutionary novelties are poorly understood. The gnathostome jaw joint is such a novelty, and the incorporation of bapx1 expression into the intermediate first pharyngeal arch may have played a major role in the evolution of this joint. Knockdown experiments revealed that loss of bapx1 function leads to the loss of the jaw joint, because Meckel’s cartilage and the palatoquadrate fuse during development. We used Xenopus laevis and Ambystoma mexicanum to further investigate the function of bapx1 in amphibians. Bapx1 expression levels were upregulated through the use of Ly-294,002 and we investigated the potential consequences of the enhanced bapx1 expression in amphibians to test the hypothesized joint inducing function of bapx1. RESULTS: We show that Ly-294,002 upregulates bapx1 expression in vivo. Additionally, ectopic mandibular arch derived cartilages develop after Ly-294,002 treatment. These ectopic cartilages are dorsoventrally oriented rods situated lateral to the palatoquadrate. The development of these additional cartilages did not change the muscular arrangement of mandibular arch-derived muscles. CONCLUSIONS: Development of additional mandibular cartilages is not unusual in larval anurans. Therefore, changes in the bapx1 expression during evolution may have been the reason for the development of several additional cartilages in the larval anuran jaw. Furthermore, our observations imply a joint-promoting function of bapx1, which further substantiates its hypothetical role in the evolution of the gnathostome jaw joint. BioMed Central 2018-06-13 /pmc/articles/PMC5998585/ /pubmed/29942645 http://dx.doi.org/10.1186/s40851-018-0101-3 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Lukas, Paul
Olsson, Lennart
Bapx1 upregulation is associated with ectopic mandibular cartilage development in amphibians
title Bapx1 upregulation is associated with ectopic mandibular cartilage development in amphibians
title_full Bapx1 upregulation is associated with ectopic mandibular cartilage development in amphibians
title_fullStr Bapx1 upregulation is associated with ectopic mandibular cartilage development in amphibians
title_full_unstemmed Bapx1 upregulation is associated with ectopic mandibular cartilage development in amphibians
title_short Bapx1 upregulation is associated with ectopic mandibular cartilage development in amphibians
title_sort bapx1 upregulation is associated with ectopic mandibular cartilage development in amphibians
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5998585/
https://www.ncbi.nlm.nih.gov/pubmed/29942645
http://dx.doi.org/10.1186/s40851-018-0101-3
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