Loss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway

Elongator dysfunction is increasingly recognized as a contributor to multiple neurodevelopmental and neurodegenerative disorders including familial dysautonomia, intellectual disability, amyotrophic lateral sclerosis, and autism spectrum disorder. Although numerous cellular processes are perturbed i...

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Autores principales:	BreAnna Cameron, Elin Lehrmann, Tien Chih, Joseph Walters, Richard Buksch, Sara Snyder, Joy Goffena, Frances Lefcort, Kevin G. Becker, Lynn George
Formato:	article
Lenguaje:	EN
Publicado:	The Company of Biologists 2021
Materias:	elongator elp1 h2a.z histone tsa notch Science Q Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/f10f606d983743c4bc6ad48340bb8bb1
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spelling	oai:doaj.org-article:f10f606d983743c4bc6ad48340bb8bb12021-11-28T16:01:29ZLoss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway2046-639010.1242/bio.058979https://doaj.org/article/f10f606d983743c4bc6ad48340bb8bb12021-09-01T00:00:00Zhttp://bio.biologists.org/content/10/9/bio058979https://doaj.org/toc/2046-6390Elongator dysfunction is increasingly recognized as a contributor to multiple neurodevelopmental and neurodegenerative disorders including familial dysautonomia, intellectual disability, amyotrophic lateral sclerosis, and autism spectrum disorder. Although numerous cellular processes are perturbed in the context of Elongator loss, converging evidence from multiple studies has resolved Elongator's primary function in the cell to the modification of tRNA wobble uridines and the translational regulation of codon-biased genes. Here we characterize H2a.z, encoding the variant H2a histone H2A.Z, as an indirect Elongator target. We further show that canonical Notch signaling, a pathway directed by H2A.Z, is perturbed as a consequence of Elp1 loss. Finally, we demonstrate that hyperacetylation of H2A.Z and other histones via exposure to the histone deacetylase inhibitor Trichostatin A during neurogenesis corrects the expression of Notch3 and rescues the development of sensory neurons in embryos lacking the Elp1 Elongator subunit.BreAnna CameronElin LehrmannTien ChihJoseph WaltersRichard BukschSara SnyderJoy GoffenaFrances LefcortKevin G. BeckerLynn GeorgeThe Company of Biologistsarticleelongatorelp1h2a.zhistonetsanotchScienceQBiology (General)QH301-705.5ENBiology Open, Vol 10, Iss 9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	elongator elp1 h2a.z histone tsa notch Science Q Biology (General) QH301-705.5
spellingShingle	elongator elp1 h2a.z histone tsa notch Science Q Biology (General) QH301-705.5 BreAnna Cameron Elin Lehrmann Tien Chih Joseph Walters Richard Buksch Sara Snyder Joy Goffena Frances Lefcort Kevin G. Becker Lynn George Loss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway
description	Elongator dysfunction is increasingly recognized as a contributor to multiple neurodevelopmental and neurodegenerative disorders including familial dysautonomia, intellectual disability, amyotrophic lateral sclerosis, and autism spectrum disorder. Although numerous cellular processes are perturbed in the context of Elongator loss, converging evidence from multiple studies has resolved Elongator's primary function in the cell to the modification of tRNA wobble uridines and the translational regulation of codon-biased genes. Here we characterize H2a.z, encoding the variant H2a histone H2A.Z, as an indirect Elongator target. We further show that canonical Notch signaling, a pathway directed by H2A.Z, is perturbed as a consequence of Elp1 loss. Finally, we demonstrate that hyperacetylation of H2A.Z and other histones via exposure to the histone deacetylase inhibitor Trichostatin A during neurogenesis corrects the expression of Notch3 and rescues the development of sensory neurons in embryos lacking the Elp1 Elongator subunit.
format	article
author	BreAnna Cameron Elin Lehrmann Tien Chih Joseph Walters Richard Buksch Sara Snyder Joy Goffena Frances Lefcort Kevin G. Becker Lynn George
author_facet	BreAnna Cameron Elin Lehrmann Tien Chih Joseph Walters Richard Buksch Sara Snyder Joy Goffena Frances Lefcort Kevin G. Becker Lynn George
author_sort	BreAnna Cameron
title	Loss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway
title_short	Loss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway
title_full	Loss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway
title_fullStr	Loss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway
title_full_unstemmed	Loss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway
title_sort	loss of elp1 perturbs histone h2a.z and the notch signaling pathway
publisher	The Company of Biologists
publishDate	2021
url	https://doaj.org/article/f10f606d983743c4bc6ad48340bb8bb1
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Loss of Elp1 perturbs histone H2A.Z and the Notch signaling pathway

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