Control of type-D GABAergic neuron differentiation by C. elegans UNC-30 homeodomain protein

Abstract

The Caenorhabditis elegans gene unc-30 is required for the development and functioning of the 19 inhibitory GABAergic (gamma-aminobutyric-acid-secreting) type D motor neurons, which control locomotion. In unc-30 mutants the D neurons lack GABA and have defects in axonal pathfinding and synaptic connections (J. White, personal communication). We report here that unc-30 encodes a homeodomain protein that is present in the nuclei of the D neurons at high levels in young larvae, in which the motor circuitry is formed, and at low levels in older animals. The UNC-30 protein is also present in six non-GABAergic neurons and is absent from the seven non-D-type GABAergic neurons. Ectopic expression of unc-30 induced GABA expression in cells that are normally not GABAergic. We propose that unc-30 functions as a transcriptional regulator within the type D neurons to control their terminal differentiation and that unc-30 is sufficient in some but not all cell types to induce GABA expression.