REST is the main negative regulator of endocrine differentiation during pancreatic organogenesis

A research team discovered the role of a gene that is essential for increasing the number of insulin-producing cells during the early development of the pancreas

Researchers from the Center for Genome Regulation (CRG), Bellvitge Institute for Biomedical Research (IDIBELL), and the University of Barcelona have studied the RE1 silent transcription factor gene, also known as REST, in mouse and zebrafish models and human pancreatic organoids

They found that REST is expressed in undifferentiated embryonic pancreatic cells (also called progenitor cells) and adult cells that form pancreatic ducts

Experiments with mouse models have shown that knocking out the REST gene in the early embryonic stage, before the pancreas is formed, will double the number of insulin-producing cells

After the pancreas has formed, the inactivation of REST cannot promote the formation of beta cells

"Although REST is important for the development of the pancreas, we have proven that REST is not the only guardian of endocrine differentiation

New therapies and treatments can increase or replace the number of insulin-producing cells in the pancreas, which will change the treatment of diabetes.

"REST is one of the dominant inhibitors of endocrine differentiation during pancreatic development," said Meritxell Rovira, a co-author of the study and a researcher in collaboration with IDIBELL and the University of Barcelona

DOI

10.

Article title

REST is a major negative regulator of endocrine differentiation during pancreas organogenesis