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

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans. / Romanos, Teresa Rojo; Pladevall-Morera, David; Langebeck-Jensen, Kasper; Hansen, Stine; Ng, Leelee; Pocock, Roger.

In: Scientific Reports, Vol. 7, No. 1, 7294, 2017.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Romanos, TR, Pladevall-Morera, D, Langebeck-Jensen, K, Hansen, S, Ng, L & Pocock, R 2017, 'LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans', Scientific Reports, vol. 7, no. 1, 7294. https://doi.org/10.1038/s41598-017-07876-4

APA

Romanos, T. R., Pladevall-Morera, D., Langebeck-Jensen, K., Hansen, S., Ng, L., & Pocock, R. (2017). LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans. Scientific Reports, 7(1), [7294]. https://doi.org/10.1038/s41598-017-07876-4

Vancouver

Romanos TR, Pladevall-Morera D, Langebeck-Jensen K, Hansen S, Ng L, Pocock R. LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans. Scientific Reports. 2017;7(1). 7294. https://doi.org/10.1038/s41598-017-07876-4

Author

Romanos, Teresa Rojo ; Pladevall-Morera, David ; Langebeck-Jensen, Kasper ; Hansen, Stine ; Ng, Leelee ; Pocock, Roger. / LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans. In: Scientific Reports. 2017 ; Vol. 7, No. 1.

Bibtex

@article{b5ea575d15c24032b180add6a865aa97,
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",
year = "2017",
doi = "10.1038/s41598-017-07876-4",
language = "English",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

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.

U2 - 10.1038/s41598-017-07876-4

DO - 10.1038/s41598-017-07876-4

M3 - Journal article

C2 - 28779171

AN - SCOPUS:85026829389

VL - 7

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

M1 - 7294

ER -

ID: 184606187