Rfx6 promotes the differentiation of peptide-secreting enteroendocrine cells while repressing genetic programs controlling serotonin production.
Fiche publication
Date publication
novembre 2019
Journal
Molecular metabolism
Auteurs
Membres identifiés du Cancéropôle Est :
Dr DE ARCANGELIS Adèle, Dr GRADWOHL Gérard, Dr SCHREIBER Valérie, Mme THIBAULT-CARPENTIER Christelle, Dr MOLINA Nacho
Tous les auteurs :
Piccand J, Vagne C, Blot F, Meunier A, Beucher A, Strasser P, Lund ML, Ghimire S, Nivlet L, Lapp C, Petersen N, Engelstoft MS, Thibault-Carpentier C, Keime C, Correa SJ, Schreiber V, Molina N, Schwartz TW, De Arcangelis A, Gradwohl G
Lien Pubmed
Résumé
Enteroendocrine cells (EECs) of the gastro-intestinal tract sense gut luminal factors and release peptide hormones or serotonin (5-HT) to coordinate energy uptake and storage. Our goal is to decipher the gene regulatory networks controlling EECs specification from enteroendocrine progenitors. In this context, we studied the role of the transcription factor Rfx6 which had been identified as the cause of Mitchell-Riley syndrome, characterized by neonatal diabetes and congenital malabsorptive diarrhea. We previously reported that Rfx6 was essential for pancreatic beta cell development and function; however, the role of Rfx6 in EECs differentiation remained to be elucidated.
Mots clés
Cell fate, Enterochromaffin cells, Enteroendocrine cells, Intestine, Lmx1a, Malabsorption, Mitchell–Riley syndrome, Neurog3, Rfx6, Serotonin
Référence
Mol Metab. 2019 Nov;29:24-39