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 develop-ment and functioning of the 19 inhibitory GABAergic (γ-aminobutyric-acid-secreting) type D motor neurons, which control locomotion^1–4. In unc-30 mutants the D neurons lack GAB A2 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 cir-cuitry is formed, and at low levels in older animals. The UNC-30 protein is also present in six non-G A B Aergic neurons and is absent from the seven non-D-type GABAergic neurons. Ectopic expres-sion of unc-30 induced GABA expression in cells that are normally not GABAergic. We propose that unc-30 functions as a transcrip-tional 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.