ArticleScientific reports2017
LIN-32/Atonal Controls Oxygen Sensing Neuron Development in Caenorhabditis elegans.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- A gene expression atlas of a juvenile nervous system.bioRxiv : the preprint server for biology · 2025Article
- Neurogenesis in Caenorhabditis elegans.Genetics · 2024Review
- Article
- Lineage-specific control of convergent differentiation by a Forkhead repressor.Development (Cambridge, England) · 2021Article
- Piecemeal regulation of convergent neuronal lineages by bHLH transcription factors in Caenorhabditis elegans.Development (Cambridge, England) · 2021Article
- Regulation of Gliogenesis byG3 (Bethesda, Md.) · 2020Article
- Behavioral Assays to Study Oxygen and Carbon Dioxide Sensing inBio-protocol · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
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.
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Registered trials
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