is required to specify a subset of ventromedial hypothalamic neurons.

Despite clear physiological roles, the ventromedial hypothalamus (VMH) developmental programs are poorly understood. Here, we asked whether the proneural gene achaete-scute homolog 1 () contributes to VMH development. transcripts were detected in embryonic day (E) 10.5 to postnatal day 0 VMH neural progenitors. The elimination of reduced the number of VMH neurons at E12.5 and E15.5, particularly within the VMH-central (VMH) and -dorsomedial (VMH) subdomains, and resulted in a VMH cell fate change from glutamatergic to GABAergic. We observed a loss of expression in hypothalamic progenitors and an upregulation of when was overexpressed. We also demonstrated a glutamatergic to GABAergic fate switch in -null mutant mice, suggesting that might act via to drive VMH cell fate decisions. We also showed a concomitant increase in expression of the central GABAergic fate determinant in the null hypothalamus. However, was not sufficient to induce an ectopic VMH fate when overexpressed outside the normal window of competency. Combined, is required but not sufficient to specify the neurotransmitter identity of VMH neurons, acting in a transcriptional cascade with .