is required to specify a subset of ventromedial hypothalamic neurons.
Fiche publication
Date publication
avril 2020
Journal
Development (Cambridge, England)
Auteurs
Membres identifiés du Cancéropôle Est :
Dr GRADWOHL Gérard
Tous les auteurs :
Aslanpour S, Rosin JM, Balakrishnan A, Klenin N, Blot F, Gradwohl G, Schuurmans C, Kurrasch DM
Lien Pubmed
Résumé
Despite clear physiological roles, the ventromedial hypothalamus (VMH) developmental programs are poorly understood. Here, we asked whether the proneural gene, (), contributes to VMH development. transcripts were detected in E10.5-P0 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 mutant mice suggesting that might act via to drive VMH cell fate decisions. We also showed a concomitant increase in the central GABAergic fate determinant expression in the null hypothalamus. However, was not sufficient to induce an ectopic VMH fate when overexpressed outside of 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 .
Mots clés
Ascl1, Cell fate decision, Differentiation, Neurog3, Ventromedial Hypothalamus
Référence
Development. 2020 Apr 6;: