The ADAMTS5 Metzincin Regulates Zebrafish Somite Differentiation

The ADAMTS5 metzincin, a secreted zinc-dependent metalloproteinase, modulates the extracellular matrix (ECM) during limb morphogenesis and other developmental processes. Here, the role of ADAMTS5 was investigated by knockdown of zebrafish adamts5 during embryogenesis. This revealed impaired Sonic He...

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Autores principales: Dancevic, Carolyn M., Gibert, Yann, Berger, Joachim, Smith, Adam D., Liongue, Clifford, Stupka, Nicole, Ward, Alister C., McCulloch, Daniel R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877627/
https://www.ncbi.nlm.nih.gov/pubmed/29518972
http://dx.doi.org/10.3390/ijms19030766
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author Dancevic, Carolyn M.
Gibert, Yann
Berger, Joachim
Smith, Adam D.
Liongue, Clifford
Stupka, Nicole
Ward, Alister C.
McCulloch, Daniel R.
author_facet Dancevic, Carolyn M.
Gibert, Yann
Berger, Joachim
Smith, Adam D.
Liongue, Clifford
Stupka, Nicole
Ward, Alister C.
McCulloch, Daniel R.
author_sort Dancevic, Carolyn M.
collection PubMed
description The ADAMTS5 metzincin, a secreted zinc-dependent metalloproteinase, modulates the extracellular matrix (ECM) during limb morphogenesis and other developmental processes. Here, the role of ADAMTS5 was investigated by knockdown of zebrafish adamts5 during embryogenesis. This revealed impaired Sonic Hedgehog (Shh) signaling during somite patterning and early myogenesis. Notably, synergistic regulation of myod expression by ADAMTS5 and Shh during somite differentiation was observed. These roles were not dependent upon the catalytic activity of ADAMTS5. These data identify a non-enzymatic function for ADAMTS5 in regulating an important cell signaling pathway that impacts on muscle development, with implications for musculoskeletal diseases in which ADAMTS5 and Shh have been associated.
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spelling pubmed-58776272018-04-09 The ADAMTS5 Metzincin Regulates Zebrafish Somite Differentiation Dancevic, Carolyn M. Gibert, Yann Berger, Joachim Smith, Adam D. Liongue, Clifford Stupka, Nicole Ward, Alister C. McCulloch, Daniel R. Int J Mol Sci Article The ADAMTS5 metzincin, a secreted zinc-dependent metalloproteinase, modulates the extracellular matrix (ECM) during limb morphogenesis and other developmental processes. Here, the role of ADAMTS5 was investigated by knockdown of zebrafish adamts5 during embryogenesis. This revealed impaired Sonic Hedgehog (Shh) signaling during somite patterning and early myogenesis. Notably, synergistic regulation of myod expression by ADAMTS5 and Shh during somite differentiation was observed. These roles were not dependent upon the catalytic activity of ADAMTS5. These data identify a non-enzymatic function for ADAMTS5 in regulating an important cell signaling pathway that impacts on muscle development, with implications for musculoskeletal diseases in which ADAMTS5 and Shh have been associated. MDPI 2018-03-07 /pmc/articles/PMC5877627/ /pubmed/29518972 http://dx.doi.org/10.3390/ijms19030766 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Dancevic, Carolyn M.
Gibert, Yann
Berger, Joachim
Smith, Adam D.
Liongue, Clifford
Stupka, Nicole
Ward, Alister C.
McCulloch, Daniel R.
The ADAMTS5 Metzincin Regulates Zebrafish Somite Differentiation
title The ADAMTS5 Metzincin Regulates Zebrafish Somite Differentiation
title_full The ADAMTS5 Metzincin Regulates Zebrafish Somite Differentiation
title_fullStr The ADAMTS5 Metzincin Regulates Zebrafish Somite Differentiation
title_full_unstemmed The ADAMTS5 Metzincin Regulates Zebrafish Somite Differentiation
title_short The ADAMTS5 Metzincin Regulates Zebrafish Somite Differentiation
title_sort adamts5 metzincin regulates zebrafish somite differentiation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877627/
https://www.ncbi.nlm.nih.gov/pubmed/29518972
http://dx.doi.org/10.3390/ijms19030766
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