EGL-13/SoxD Specifies Distinct O₂ and CO₂ Sensory Neuron Fates in <i>Caenorhabditis elegans</i>

<div><p></p><p>Animals harbor specialized neuronal systems that are used for sensing and coordinating responses to changes in oxygen (O₂) and carbon dioxide (CO₂). In <i>Caenorhabditis elegans</i>, the O₂/CO₂ sensory system comprises functionally and morphologically distinct sensory neurons that mediate rapid behavioral responses to exquisite changes in O₂ or CO₂ levels via different sensory receptors. How the diversification of the O₂- and CO₂-sensing neurons is established is poorly understood. We show here that the molecular identity of both the BAG (O₂/CO₂-sensing) and the URX (O₂-sensing) neurons is controlled by the phylogenetically conserved SoxD transcription factor homolog EGL-13. <i>egl-13</i> mutant animals fail to fully express the distinct terminal gene batteries of the BAG and URX neurons and, as such, are unable to mount behavioral responses to changes in O₂ and CO₂. We found that the expression of <i>egl-13</i> is regulated in the BAG and URX neurons by two conserved transcription factors—ETS-5(Ets factor) in the BAG neurons and AHR-1(bHLH factor) in the URX neurons. In addition, we found that EGL-13 acts in partially parallel pathways with both ETS-5 and AHR-1 to direct BAG and URX neuronal fate respectively. Finally, we found that EGL-13 is sufficient to induce O₂- and CO₂-sensing cell fates in some cellular contexts. Thus, the same core regulatory factor, <i>egl-13</i>, is required and sufficient to specify the distinct fates of O₂- and CO₂-sensing neurons in <i>C. elegans</i>. These findings extend our understanding of mechanisms of neuronal diversification and the regulation of molecular factors that may be conserved in higher organisms.</p></div