LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans

Abstract Development of complex nervous systems requires precisely controlled neurogenesis. The generation and specification of neurons occur through the transcriptional and post-transcriptional control of complex regulatory networks. In vertebrates and invertebrates, the proneural basic-helix-loop-...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Teresa Rojo Romanos, David Pladevall-Morera, Kasper Langebeck-Jensen, Stine Hansen, Leelee Ng, Roger Pocock
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/cc7c48583f414d6188cea390d016f4c9
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:cc7c48583f414d6188cea390d016f4c9
record_format	dspace
spelling	oai:doaj.org-article:cc7c48583f414d6188cea390d016f4c92021-12-02T16:06:12ZLIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans10.1038/s41598-017-07876-42045-2322https://doaj.org/article/cc7c48583f414d6188cea390d016f4c92017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07876-4https://doaj.org/toc/2045-2322Abstract Development of complex nervous systems requires precisely controlled neurogenesis. The generation and specification of neurons occur through the transcriptional and post-transcriptional control of complex regulatory networks. In vertebrates and invertebrates, the proneural basic-helix-loop-helix (bHLH) family of transcription factors has multiple functions in neurogenesis. Here, we identified the LIN-32/Atonal bHLH transcription factor as a key regulator of URXL/R oxygen-sensing neuron development in Caenorhabditis elegans. When LIN-32/Atonal expression is lost, the expression of URX specification and terminal differentiation genes is abrogated. As such, lin-32 mutant animals are unable to respond to increases in environmental oxygen. The URX neurons are generated from a branch of the cell lineage that also produces the CEPDL/R and URADL/R neurons. We found development of these neurons is also defective, suggesting that LIN-32/Atonal regulates neuronal development of the entire lineage. Finally, our results show that aspects of URX neuronal fate are partially restored in lin-32 mutant animals when the apoptosis pathway is inhibited. This suggests that, as in other organisms, LIN-32/Atonal regulates neuronal apoptosis.Teresa Rojo RomanosDavid Pladevall-MoreraKasper Langebeck-JensenStine HansenLeelee NgRoger PocockNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Teresa Rojo Romanos David Pladevall-Morera Kasper Langebeck-Jensen Stine Hansen Leelee Ng Roger Pocock LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans
description	Abstract Development of complex nervous systems requires precisely controlled neurogenesis. The generation and specification of neurons occur through the transcriptional and post-transcriptional control of complex regulatory networks. In vertebrates and invertebrates, the proneural basic-helix-loop-helix (bHLH) family of transcription factors has multiple functions in neurogenesis. Here, we identified the LIN-32/Atonal bHLH transcription factor as a key regulator of URXL/R oxygen-sensing neuron development in Caenorhabditis elegans. When LIN-32/Atonal expression is lost, the expression of URX specification and terminal differentiation genes is abrogated. As such, lin-32 mutant animals are unable to respond to increases in environmental oxygen. The URX neurons are generated from a branch of the cell lineage that also produces the CEPDL/R and URADL/R neurons. We found development of these neurons is also defective, suggesting that LIN-32/Atonal regulates neuronal development of the entire lineage. Finally, our results show that aspects of URX neuronal fate are partially restored in lin-32 mutant animals when the apoptosis pathway is inhibited. This suggests that, as in other organisms, LIN-32/Atonal regulates neuronal apoptosis.
format	article
author	Teresa Rojo Romanos David Pladevall-Morera Kasper Langebeck-Jensen Stine Hansen Leelee Ng Roger Pocock
author_facet	Teresa Rojo Romanos David Pladevall-Morera Kasper Langebeck-Jensen Stine Hansen Leelee Ng Roger Pocock
author_sort	Teresa Rojo Romanos
title	LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans
title_short	LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans
title_full	LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans
title_fullStr	LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans
title_full_unstemmed	LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans
title_sort	lin-32/atonal controls oxygen sensing neuron development in caenorhabditis elegans
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/cc7c48583f414d6188cea390d016f4c9
work_keys_str_mv	AT teresarojoromanos lin32atonalcontrolsoxygensensingneurondevelopmentincaenorhabditiselegans AT davidpladevallmorera lin32atonalcontrolsoxygensensingneurondevelopmentincaenorhabditiselegans AT kasperlangebeckjensen lin32atonalcontrolsoxygensensingneurondevelopmentincaenorhabditiselegans AT stinehansen lin32atonalcontrolsoxygensensingneurondevelopmentincaenorhabditiselegans AT leeleeng lin32atonalcontrolsoxygensensingneurondevelopmentincaenorhabditiselegans AT rogerpocock lin32atonalcontrolsoxygensensingneurondevelopmentincaenorhabditiselegans
_version_	1718385114426114048

LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans

Ejemplares similares