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

Teresa Rojo Romanos; David Pladevall-Morera; Kasper Langebeck-Jensen; Stine Hansen; Leelee Ng; Roger Pocock

doi:10.1038/s41598-017-07876-4

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

Teresa Rojo Romanos, David Pladevall-Morera, Kasper Langebeck-Jensen, Stine Hansen, Leelee Ng, Roger Pocock^*

^*Corresponding author for this work

1 Citation (Scopus)

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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.

Original language	English
Article number	7294
Journal	Scientific Reports
Volume	7
Issue number	1
Number of pages	10
ISSN	2045-2322
DOIs	https://doi.org/10.1038/s41598-017-07876-4
Publication status	Published - 2017

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LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegansFinal published version, 1.67 MBLicence: CC BY

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title = "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-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.",

author = "Romanos, {Teresa Rojo} and David Pladevall-Morera and Kasper Langebeck-Jensen and Stine Hansen and Leelee Ng and Roger Pocock",

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T1 - LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans

AU - Romanos, Teresa Rojo

AU - Pladevall-Morera, David

AU - Langebeck-Jensen, Kasper

AU - Hansen, Stine

AU - Ng, Leelee

AU - Pocock, Roger

PY - 2017

Y1 - 2017

N2 - 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.

AB - 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.

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DO - 10.1038/s41598-017-07876-4

M3 - Journal article

C2 - 28779171

AN - SCOPUS:85026829389

SN - 2045-2322

VL - 7

JO - Scientific Reports

JF - Scientific Reports

IS - 1

M1 - 7294

ER -

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

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