Beta-actin is required for proper mouse neural crest ontogeny.

The mouse genome consists of six functional actin genes of which the expression patterns are temporally and spatially regulated during development and in the adult organism. Deletion of beta-actin in mouse is lethal during embryonic development, although there is compensatory expression of other act...

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Autores principales:	Davina Tondeleir, Rivka Noelanders, Karima Bakkali, Christophe Ampe
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/fd7038d6a93e47f2bf1f930b4a4766e0
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spelling	oai:doaj.org-article:fd7038d6a93e47f2bf1f930b4a4766e02021-11-18T08:38:42ZBeta-actin is required for proper mouse neural crest ontogeny.1932-620310.1371/journal.pone.0085608https://doaj.org/article/fd7038d6a93e47f2bf1f930b4a4766e02014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24409333/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203The mouse genome consists of six functional actin genes of which the expression patterns are temporally and spatially regulated during development and in the adult organism. Deletion of beta-actin in mouse is lethal during embryonic development, although there is compensatory expression of other actin isoforms. This suggests different isoform specific functions and, more in particular, an important function for beta-actin during early mammalian development. We here report a role for beta-actin during neural crest ontogeny. Although beta-actin null neural crest cells show expression of neural crest markers, less cells delaminate and their migration arrests shortly after. These phenotypes were associated with elevated apoptosis levels in neural crest cells, whereas proliferation levels were unchanged. Specifically the pre-migratory neural crest cells displayed higher levels of apoptosis, suggesting increased apoptosis in the neural tube accounts for the decreased amount of migrating neural crest cells seen in the beta-actin null embryos. These cells additionally displayed a lack of membrane bound N-cadherin and dramatic decrease in cadherin-11 expression which was more pronounced in the pre-migratory neural crest population, potentially indicating linkage between the cadherin-11 expression and apoptosis. By inhibiting ROCK ex vivo, the knockout neural crest cells regained migratory capacity and cadherin-11 expression was upregulated. We conclude that the presence of beta-actin is vital for survival, specifically of pre-migratory neural crest cells, their proper emigration from the neural tube and their subsequent migration. Furthermore, the absence of beta-actin affects cadherin-11 and N-cadherin function, which could partly be alleviated by ROCK inhibition, situating the Rho-ROCK signaling in a feedback loop with cadherin-11.Davina TondeleirRivka NoelandersKarima BakkaliChristophe AmpePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 1, p e85608 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Davina Tondeleir Rivka Noelanders Karima Bakkali Christophe Ampe Beta-actin is required for proper mouse neural crest ontogeny.
description	The mouse genome consists of six functional actin genes of which the expression patterns are temporally and spatially regulated during development and in the adult organism. Deletion of beta-actin in mouse is lethal during embryonic development, although there is compensatory expression of other actin isoforms. This suggests different isoform specific functions and, more in particular, an important function for beta-actin during early mammalian development. We here report a role for beta-actin during neural crest ontogeny. Although beta-actin null neural crest cells show expression of neural crest markers, less cells delaminate and their migration arrests shortly after. These phenotypes were associated with elevated apoptosis levels in neural crest cells, whereas proliferation levels were unchanged. Specifically the pre-migratory neural crest cells displayed higher levels of apoptosis, suggesting increased apoptosis in the neural tube accounts for the decreased amount of migrating neural crest cells seen in the beta-actin null embryos. These cells additionally displayed a lack of membrane bound N-cadherin and dramatic decrease in cadherin-11 expression which was more pronounced in the pre-migratory neural crest population, potentially indicating linkage between the cadherin-11 expression and apoptosis. By inhibiting ROCK ex vivo, the knockout neural crest cells regained migratory capacity and cadherin-11 expression was upregulated. We conclude that the presence of beta-actin is vital for survival, specifically of pre-migratory neural crest cells, their proper emigration from the neural tube and their subsequent migration. Furthermore, the absence of beta-actin affects cadherin-11 and N-cadherin function, which could partly be alleviated by ROCK inhibition, situating the Rho-ROCK signaling in a feedback loop with cadherin-11.
format	article
author	Davina Tondeleir Rivka Noelanders Karima Bakkali Christophe Ampe
author_facet	Davina Tondeleir Rivka Noelanders Karima Bakkali Christophe Ampe
author_sort	Davina Tondeleir
title	Beta-actin is required for proper mouse neural crest ontogeny.
title_short	Beta-actin is required for proper mouse neural crest ontogeny.
title_full	Beta-actin is required for proper mouse neural crest ontogeny.
title_fullStr	Beta-actin is required for proper mouse neural crest ontogeny.
title_full_unstemmed	Beta-actin is required for proper mouse neural crest ontogeny.
title_sort	beta-actin is required for proper mouse neural crest ontogeny.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/fd7038d6a93e47f2bf1f930b4a4766e0
work_keys_str_mv	AT davinatondeleir betaactinisrequiredforpropermouseneuralcrestontogeny AT rivkanoelanders betaactinisrequiredforpropermouseneuralcrestontogeny AT karimabakkali betaactinisrequiredforpropermouseneuralcrestontogeny AT christopheampe betaactinisrequiredforpropermouseneuralcrestontogeny
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Beta-actin is required for proper mouse neural crest ontogeny.

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