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Trpc1 as the Missing Link Between the Bmp and Ca(2+) Signalling Pathways During Neural Specification in Amphibians
In amphibians, the inhibition of bone morphogenetic protein (BMP) in the dorsal ectoderm has been proposed to be responsible for the first step of neural specification, called neural induction. We previously demonstrated that in Xenopus laevis embryos, the BMP signalling antagonist, noggin, triggers...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6831629/ https://www.ncbi.nlm.nih.gov/pubmed/31690785 http://dx.doi.org/10.1038/s41598-019-52556-0 |
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author | Néant, Isabelle Leung, Ho Chi Webb, Sarah E. Miller, Andrew L. Moreau, Marc Leclerc, Catherine |
author_facet | Néant, Isabelle Leung, Ho Chi Webb, Sarah E. Miller, Andrew L. Moreau, Marc Leclerc, Catherine |
author_sort | Néant, Isabelle |
collection | PubMed |
description | In amphibians, the inhibition of bone morphogenetic protein (BMP) in the dorsal ectoderm has been proposed to be responsible for the first step of neural specification, called neural induction. We previously demonstrated that in Xenopus laevis embryos, the BMP signalling antagonist, noggin, triggers an influx of Ca(2+) through voltage-dependent L-type Ca(2+) channels (LTCCs), mainly via Ca(V)1.2, and we showed that this influx constitutes a necessary and sufficient signal for triggering the expression of neural genes. However, the mechanism linking the inhibition of BMP signalling with the activation of LTCCs remained unknown. Here, we demonstrate that the transient receptor potential canonical subfamily member 1, (Trpc1), is an intermediate between BMP receptor type II (BMPRII) and the Ca(V)1.2 channel. We show that noggin induces a physical interaction between BMPRII and Trpc1 channels. This interaction leads to the activation of Trpc1 channels and to an influx of cations, which depolarizes the plasma membrane up to a threshold sufficient to activate Cav1.2. Together, our results demonstrate for the first time that during neural induction, Ca(2+) entry through the Ca(V)1.2 channel results from the noggin-induced interaction between Trpc1 and BMPRII. |
format | Online Article Text |
id | pubmed-6831629 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-68316292019-11-13 Trpc1 as the Missing Link Between the Bmp and Ca(2+) Signalling Pathways During Neural Specification in Amphibians Néant, Isabelle Leung, Ho Chi Webb, Sarah E. Miller, Andrew L. Moreau, Marc Leclerc, Catherine Sci Rep Article In amphibians, the inhibition of bone morphogenetic protein (BMP) in the dorsal ectoderm has been proposed to be responsible for the first step of neural specification, called neural induction. We previously demonstrated that in Xenopus laevis embryos, the BMP signalling antagonist, noggin, triggers an influx of Ca(2+) through voltage-dependent L-type Ca(2+) channels (LTCCs), mainly via Ca(V)1.2, and we showed that this influx constitutes a necessary and sufficient signal for triggering the expression of neural genes. However, the mechanism linking the inhibition of BMP signalling with the activation of LTCCs remained unknown. Here, we demonstrate that the transient receptor potential canonical subfamily member 1, (Trpc1), is an intermediate between BMP receptor type II (BMPRII) and the Ca(V)1.2 channel. We show that noggin induces a physical interaction between BMPRII and Trpc1 channels. This interaction leads to the activation of Trpc1 channels and to an influx of cations, which depolarizes the plasma membrane up to a threshold sufficient to activate Cav1.2. Together, our results demonstrate for the first time that during neural induction, Ca(2+) entry through the Ca(V)1.2 channel results from the noggin-induced interaction between Trpc1 and BMPRII. Nature Publishing Group UK 2019-11-05 /pmc/articles/PMC6831629/ /pubmed/31690785 http://dx.doi.org/10.1038/s41598-019-52556-0 Text en © The Author(s) 2019 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 Néant, Isabelle Leung, Ho Chi Webb, Sarah E. Miller, Andrew L. Moreau, Marc Leclerc, Catherine Trpc1 as the Missing Link Between the Bmp and Ca(2+) Signalling Pathways During Neural Specification in Amphibians |
title | Trpc1 as the Missing Link Between the Bmp and Ca(2+) Signalling Pathways During Neural Specification in Amphibians |
title_full | Trpc1 as the Missing Link Between the Bmp and Ca(2+) Signalling Pathways During Neural Specification in Amphibians |
title_fullStr | Trpc1 as the Missing Link Between the Bmp and Ca(2+) Signalling Pathways During Neural Specification in Amphibians |
title_full_unstemmed | Trpc1 as the Missing Link Between the Bmp and Ca(2+) Signalling Pathways During Neural Specification in Amphibians |
title_short | Trpc1 as the Missing Link Between the Bmp and Ca(2+) Signalling Pathways During Neural Specification in Amphibians |
title_sort | trpc1 as the missing link between the bmp and ca(2+) signalling pathways during neural specification in amphibians |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6831629/ https://www.ncbi.nlm.nih.gov/pubmed/31690785 http://dx.doi.org/10.1038/s41598-019-52556-0 |
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