Nucleocytoplasmic Shuttling of Histone Deacetylase 9 Controls Activity-Dependent Thalamocortical Axon Branching

Abstract During development, thalamocortical (TC) axons form branches in an activity-dependent fashion. Here we investigated how neuronal activity is converted to molecular signals, focusing on an epigenetic mechanism involving histone deacetylases (HDACs). Immunohistochemistry demonstrated that HDA...

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Autores principales:	Ricardo Alchini, Haruka Sato, Naoyuki Matsumoto, Tomomi Shimogori, Noriyuki Sugo, Nobuhiko Yamamoto
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/395131c25061436dbca24b8a988bdd92
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spelling	oai:doaj.org-article:395131c25061436dbca24b8a988bdd922021-12-02T11:41:12ZNucleocytoplasmic Shuttling of Histone Deacetylase 9 Controls Activity-Dependent Thalamocortical Axon Branching10.1038/s41598-017-06243-72045-2322https://doaj.org/article/395131c25061436dbca24b8a988bdd922017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06243-7https://doaj.org/toc/2045-2322Abstract During development, thalamocortical (TC) axons form branches in an activity-dependent fashion. Here we investigated how neuronal activity is converted to molecular signals, focusing on an epigenetic mechanism involving histone deacetylases (HDACs). Immunohistochemistry demonstrated that HDAC9 was translocated from the nucleus to the cytoplasm of thalamic cells during the first postnatal week in rats. In organotypic co-cultures of the thalamus and cortex, fluorescent protein-tagged HDAC9 also exhibited nuclueocytoplasmic translocation in thalamic cells during culturing, which was reversed by tetrodotoxin treatment. Transfection with a mutant HDAC9 that interferes with the translocation markedly decreased TC axon branching in the culture. Similarly, TC axon branching was significantly decreased by the mutant HDAC9 gene transfer in vivo. However, axonal branching was restored by disrupting the interaction between HDAC9 and myocyte-specific enhancer factor 2 (MEF2). Taken together, the present results demonstrate that the nucleocytoplasmic translocation of HDAC9 plays a critical role in activity-dependent TC axon branching by affecting transcriptional regulation and downstream signaling pathways.Ricardo AlchiniHaruka SatoNaoyuki MatsumotoTomomi ShimogoriNoriyuki SugoNobuhiko YamamotoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ricardo Alchini Haruka Sato Naoyuki Matsumoto Tomomi Shimogori Noriyuki Sugo Nobuhiko Yamamoto Nucleocytoplasmic Shuttling of Histone Deacetylase 9 Controls Activity-Dependent Thalamocortical Axon Branching
description	Abstract During development, thalamocortical (TC) axons form branches in an activity-dependent fashion. Here we investigated how neuronal activity is converted to molecular signals, focusing on an epigenetic mechanism involving histone deacetylases (HDACs). Immunohistochemistry demonstrated that HDAC9 was translocated from the nucleus to the cytoplasm of thalamic cells during the first postnatal week in rats. In organotypic co-cultures of the thalamus and cortex, fluorescent protein-tagged HDAC9 also exhibited nuclueocytoplasmic translocation in thalamic cells during culturing, which was reversed by tetrodotoxin treatment. Transfection with a mutant HDAC9 that interferes with the translocation markedly decreased TC axon branching in the culture. Similarly, TC axon branching was significantly decreased by the mutant HDAC9 gene transfer in vivo. However, axonal branching was restored by disrupting the interaction between HDAC9 and myocyte-specific enhancer factor 2 (MEF2). Taken together, the present results demonstrate that the nucleocytoplasmic translocation of HDAC9 plays a critical role in activity-dependent TC axon branching by affecting transcriptional regulation and downstream signaling pathways.
format	article
author	Ricardo Alchini Haruka Sato Naoyuki Matsumoto Tomomi Shimogori Noriyuki Sugo Nobuhiko Yamamoto
author_facet	Ricardo Alchini Haruka Sato Naoyuki Matsumoto Tomomi Shimogori Noriyuki Sugo Nobuhiko Yamamoto
author_sort	Ricardo Alchini
title	Nucleocytoplasmic Shuttling of Histone Deacetylase 9 Controls Activity-Dependent Thalamocortical Axon Branching
title_short	Nucleocytoplasmic Shuttling of Histone Deacetylase 9 Controls Activity-Dependent Thalamocortical Axon Branching
title_full	Nucleocytoplasmic Shuttling of Histone Deacetylase 9 Controls Activity-Dependent Thalamocortical Axon Branching
title_fullStr	Nucleocytoplasmic Shuttling of Histone Deacetylase 9 Controls Activity-Dependent Thalamocortical Axon Branching
title_full_unstemmed	Nucleocytoplasmic Shuttling of Histone Deacetylase 9 Controls Activity-Dependent Thalamocortical Axon Branching
title_sort	nucleocytoplasmic shuttling of histone deacetylase 9 controls activity-dependent thalamocortical axon branching
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/395131c25061436dbca24b8a988bdd92
work_keys_str_mv	AT ricardoalchini nucleocytoplasmicshuttlingofhistonedeacetylase9controlsactivitydependentthalamocorticalaxonbranching AT harukasato nucleocytoplasmicshuttlingofhistonedeacetylase9controlsactivitydependentthalamocorticalaxonbranching AT naoyukimatsumoto nucleocytoplasmicshuttlingofhistonedeacetylase9controlsactivitydependentthalamocorticalaxonbranching AT tomomishimogori nucleocytoplasmicshuttlingofhistonedeacetylase9controlsactivitydependentthalamocorticalaxonbranching AT noriyukisugo nucleocytoplasmicshuttlingofhistonedeacetylase9controlsactivitydependentthalamocorticalaxonbranching AT nobuhikoyamamoto nucleocytoplasmicshuttlingofhistonedeacetylase9controlsactivitydependentthalamocorticalaxonbranching
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Nucleocytoplasmic Shuttling of Histone Deacetylase 9 Controls Activity-Dependent Thalamocortical Axon Branching

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