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.
Highlights
We study the URXL/R body cavity neurons in C. elegans as a model for neuronal development
We found that LIN-32 is required for the expression of terminal fate reporters for other neurons generated from the URX sublineage (URADL/R and CEPDL/R), indicating that neuronal development within the entire sublineage is defective
Loss of flp-8::GFP expression in the URX neurons was phenocopied in the lin-32(tm1446) mutant strain showing that LIN-32 is important for URX development (Fig. 1C)
Summary
We study the URXL/R body cavity neurons in C. elegans as a model for neuronal development. These neurons regulate multiple aspects of animal behaviour and physiology[18,19]. We and others previously found that expression of terminal fate reporters for URX neuron fate is regulated by the Sox transcription factor EGL-13 and the AHR-1/aryl hydrocarbon receptor[21,22]. In lin-32 mutant animals, reporters for URX-expressed transcription factors, including EGL-13, and terminal differentiation genes are abrogated. We found that LIN-32 is required for the expression of terminal fate reporters for other neurons generated from the URX sublineage (URADL/R and CEPDL/R), indicating that neuronal development within the entire sublineage is defective. Our study has revealed a previously unappreciated function of LIN32/Atonal in regulating O2-sensing neuron development in the brain
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