|Start Date / Time||March 4, 2015 at 9:00 AM|
|End Date / Time||March 4, 2015 at 9:55 AM|
|Location||512 Light Hall|
|Presenter Name||Chen Huang (Gu's lab)|
|Presentation Title||Loss of Myt factors compromises postnatal beta-cell differentiation and survival|
|Status||This meeting has already occurred|
In vitro generation of beta cell has become an ideal source for transplantation-based therapy against diabetes. However, long-term challenge remains in obtaining fully functional and long-lived beta cells, necessitating a comprehensive understanding of postnatal beta cell regulation. Here we show that myelin transcription (MYT) factors are a group of genes that are required to generate and maintain mature beta cells. Pancreatic knockout of Myt factors mice exhibit overt diabetes around 1 month of age, accompanied with hugely loss of beta cell mass and compromised insulin secretion. Detailed examination found that loss of beta cell mass was caused by insufficient cell proliferation and increased cell apoptosis. Moreover, expression of a set of genes required for beta cell function is compromised in Myt mutant mice. Finally, we found Myt mutant beta cells reverse the postnatal differentiation and lose mature beta cell features. Overall, our results unravel a crucial family of genes playing a role of pro-proliferation, pro-differentiation and anti-apoptotic in postnatal beta cells.