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Myosin1D is an evolutionarily conserved regulator of animal left–right asymmetry
The establishment of left–right (LR) asymmetry is fundamental to animal development, but the identification of a unifying mechanism establishing laterality across different phyla has remained elusive. A cilia-driven, directional fluid flow is important for symmetry breaking in numerous vertebrates,...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5955935/ https://www.ncbi.nlm.nih.gov/pubmed/29769531 http://dx.doi.org/10.1038/s41467-018-04284-8 |
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author | Juan, Thomas Géminard, Charles Coutelis, Jean-Baptiste Cerezo, Delphine Polès, Sophie Noselli, Stéphane Fürthauer, Maximilian |
author_facet | Juan, Thomas Géminard, Charles Coutelis, Jean-Baptiste Cerezo, Delphine Polès, Sophie Noselli, Stéphane Fürthauer, Maximilian |
author_sort | Juan, Thomas |
collection | PubMed |
description | The establishment of left–right (LR) asymmetry is fundamental to animal development, but the identification of a unifying mechanism establishing laterality across different phyla has remained elusive. A cilia-driven, directional fluid flow is important for symmetry breaking in numerous vertebrates, including zebrafish. Alternatively, LR asymmetry can be established independently of cilia, notably through the intrinsic chirality of the acto-myosin cytoskeleton. Here, we show that Myosin1D (Myo1D), a previously identified regulator of Drosophila LR asymmetry, is essential for the formation and function of the zebrafish LR organizer (LRO), Kupffer’s vesicle (KV). Myo1D controls the orientation of LRO cilia and interacts functionally with the planar cell polarity (PCP) pathway component VanGogh-like2 (Vangl2), to shape a productive LRO flow. Our findings identify Myo1D as an evolutionarily conserved regulator of animal LR asymmetry, and show that functional interactions between Myo1D and PCP are central to the establishment of animal LR asymmetry. |
format | Online Article Text |
id | pubmed-5955935 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-59559352018-05-21 Myosin1D is an evolutionarily conserved regulator of animal left–right asymmetry Juan, Thomas Géminard, Charles Coutelis, Jean-Baptiste Cerezo, Delphine Polès, Sophie Noselli, Stéphane Fürthauer, Maximilian Nat Commun Article The establishment of left–right (LR) asymmetry is fundamental to animal development, but the identification of a unifying mechanism establishing laterality across different phyla has remained elusive. A cilia-driven, directional fluid flow is important for symmetry breaking in numerous vertebrates, including zebrafish. Alternatively, LR asymmetry can be established independently of cilia, notably through the intrinsic chirality of the acto-myosin cytoskeleton. Here, we show that Myosin1D (Myo1D), a previously identified regulator of Drosophila LR asymmetry, is essential for the formation and function of the zebrafish LR organizer (LRO), Kupffer’s vesicle (KV). Myo1D controls the orientation of LRO cilia and interacts functionally with the planar cell polarity (PCP) pathway component VanGogh-like2 (Vangl2), to shape a productive LRO flow. Our findings identify Myo1D as an evolutionarily conserved regulator of animal LR asymmetry, and show that functional interactions between Myo1D and PCP are central to the establishment of animal LR asymmetry. Nature Publishing Group UK 2018-05-16 /pmc/articles/PMC5955935/ /pubmed/29769531 http://dx.doi.org/10.1038/s41467-018-04284-8 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Juan, Thomas Géminard, Charles Coutelis, Jean-Baptiste Cerezo, Delphine Polès, Sophie Noselli, Stéphane Fürthauer, Maximilian Myosin1D is an evolutionarily conserved regulator of animal left–right asymmetry |
title | Myosin1D is an evolutionarily conserved regulator of animal left–right asymmetry |
title_full | Myosin1D is an evolutionarily conserved regulator of animal left–right asymmetry |
title_fullStr | Myosin1D is an evolutionarily conserved regulator of animal left–right asymmetry |
title_full_unstemmed | Myosin1D is an evolutionarily conserved regulator of animal left–right asymmetry |
title_short | Myosin1D is an evolutionarily conserved regulator of animal left–right asymmetry |
title_sort | myosin1d is an evolutionarily conserved regulator of animal left–right asymmetry |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5955935/ https://www.ncbi.nlm.nih.gov/pubmed/29769531 http://dx.doi.org/10.1038/s41467-018-04284-8 |
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