Poster #: 100
The Impact of Xbp1s on ER Stress and Its Role in Diabetes
Mentor: Chelsea Jang, Research Associate I
X-box binding protein 1 (Xbp1), specifically its spliced form, Xbp1s, is one of three pathways in the unfolded protein response (UPR), a response to endoplasmic reticulum (ER) stress allowing the ER to effectively adapt to stress conditions. Too much ER stress can cause beta cell dysfunction and apoptosis, resulting in diabetes. Thus, Xbp1 regulates ER function and ensures beta cell survival. The deletion of the Xbp1 gene is developmentally lethal. A mouse model was created to knock out the spliced form of the gene. Paired with other genetic mechanisms, a beta-cell specific Xbp1s knockout was created. This experiment used a mouse model with beta-cell specific Xbp1s knockout mice, and whole-body SKI-knockout and control mice. The pancreases are harvested to quantify beta cell mass as a percentage of total pancreas mass. Mice with full Xbp1-knockout or Xbp1SKI genotype are found to have lower pancreatic mass than wild or heterozygous mice.