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

https://www.ncbi.nlm.nih.gov/pubmed/31668390

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.