BME PhD Preliminary Exam Announcement for Madeline McLaughlin (C. Evans-Molina and F. Huang, co-advisors) Everyone is invited to attend the public presentation beginning at 2:00 pm. Research Title: STIM1 Interacts with G Protein-Coupled Estrogen Receptor Signaling to Maintain Beta Cell Identity in Female Mice Date: March 18, 2024 Time: 2:00 pm Place: Zoom - https://iu.zoom.us/j/8318926012<https://nam04.safelinks.protection.outlook.com/?url=https%3A%2F%2Fiu.zoom.us%2Fj%2F8318926012&data=05%7C02%7Cbmegradstudents-list%40ecn.purdue.edu%7C1a76bc3162fd4e6d06da08dc3d251c50%7C4130bd397c53419cb1e58758d6d63f21%7C0%7C0%7C638452476791618839%7CUnknown%7CTWFpbGZsb3d8eyJWIjoiMC4wLjAwMDAiLCJQIjoiV2luMzIiLCJBTiI6Ik1haWwiLCJXVCI6Mn0%3D%7C0%7C%7C%7C&sdata=cVyDIjbYOIryZ%2FezQxPt1eVHDu%2FtRMwlcZ2nJCHnzjA%3D&reserved=0> Committee Members: Dr. Carmella Evans-Molina (Co-Chair), Dr. Fang Huang (Co-Chair), Dr. Sherry Harbin, and Dr. Qing Deng Abstract: Type 2 diabetes (T2D) is a global health pandemic resulting from a combination of defective insulin secretion and impaired insulin action in peripheral tissues; however, genetic and physiologic data suggest that inadequate insulin secretion from the * cell is the chief determinant predicting T2D development. Studies have identified * cell dedifferentiation as one potential mechanism leading to * cell failure. During dedifferentiation, * cells lose expression of key identity markers and insulin secretory function and may differentiate into other endocrine cell types. At present, the molecular mechanisms leading to * cell dedifferentiation are not well understood. Calcium (Ca2+) plays a vital role in regulating * cell health and function, and the endoplasmic reticulum (ER) serves as the dominant Ca2+ store. ER Ca2+ depletion triggers the rescue mechanism store-operated Ca2+ entry (SOCE) which replenishes ER Ca2+ stores through the ER-localized Ca2+ sensor stromal interaction molecule 1 (STIM1). Our laboratory recently found that obese female mice with reduced SOCE due to * cell-specific genetic deletion of STIM1 had evidence of * cell dedifferentiation and reduced G protein coupled estrogen receptor (GPER) expression, suggesting an interaction between SOCE, GPER signaling, and * cell identity. Therefore, we hypothesize that decreased SOCE leads to reduced GPER signaling and loss of * cell identity and function, thereby contributing to the pathophysiology of T2D in females. We propose using an ovariectomy mouse model and novel imaging methods to test this hypothesis and identify a novel mechanism linking SOCE and GPER signaling to * cell failure during T2D.