Location
Havener Center, Miner Lounge / Wiese Atrium, 9:30am-11:30am
Start Date
4-1-2026 9:30 AM
End Date
4-1-2026 11:30 AM
Presentation Date
April 1, 2026; 9:30am-11:30am
Description
Prader-Willi syndrome (PWS) is a rare progressive metabolic disease characterized by a wide range of behavioral and cognitive defects, most notably severe hyperphagia. The disorder is caused by the complete loss of some paternally inherited genes on chromosome 15q11-q13, resulting in endocrine dysfunction and a loss of control over feeding behaviors. Among the deleted genes within this region is MAGEL2. Our lab recently characterized a paternally deficient MAGEL2 rat model of PWS, discovering a defect in pituitary secretory capacity that is consistent with the impaired vesicular trafficking and secretion observed in PWS patients. To further characterize the defects in vesicular trafficking in the absence of MAGEL2, we will generate a cell-based model of PWS, knocking down MAGEL2 with siRNA or knocking out MAGEL2 using CRISPR-Cas9. We have validated endosomal and vesicular antibody markers for immunofluorescence assays. These markers will later be used in cell-based models and hypothalamic tissue from PWS patients to study how the loss of MAGEL2 affects endosomal trafficking and may contribute to endocrine dysfunction.
Biography
Hayden O'Dell is an undergraduate student at Missouri S&T majoring in Biological Sciences. He is participating in the FYRE program, researching the role of GPR107 in human diabetes. His laboratory experience includes mammalian cell culture, cell passaging and maintenance, media and buffer preparation, antibody staining, and fluorescence microscopy. He also serves as a member with the iGEM team at Missouri S&T, where he has gained experience in sterile technique, media preparation, bacterial culture methods, and scientific literature review. In addition, he is a member of the Mars Rover Design Team, contributing work involved with their fluorescence microscope. His academic interests include cell biology, protein expression, and biomedical research.
Meeting Name
2026 - Miners Solving for Tomorrow Research Conference
Department(s)
Biological Sciences
Document Type
Poster
Document Version
Final Version
File Type
event
Language(s)
English
Rights
© 2026 The Authors, All rights reserved
Included in
Validating Endosomal Antibodies for Use in Immunofluorescence Assays in a Cell-Based Model of Prader Willi Syndrome
Havener Center, Miner Lounge / Wiese Atrium, 9:30am-11:30am
Prader-Willi syndrome (PWS) is a rare progressive metabolic disease characterized by a wide range of behavioral and cognitive defects, most notably severe hyperphagia. The disorder is caused by the complete loss of some paternally inherited genes on chromosome 15q11-q13, resulting in endocrine dysfunction and a loss of control over feeding behaviors. Among the deleted genes within this region is MAGEL2. Our lab recently characterized a paternally deficient MAGEL2 rat model of PWS, discovering a defect in pituitary secretory capacity that is consistent with the impaired vesicular trafficking and secretion observed in PWS patients. To further characterize the defects in vesicular trafficking in the absence of MAGEL2, we will generate a cell-based model of PWS, knocking down MAGEL2 with siRNA or knocking out MAGEL2 using CRISPR-Cas9. We have validated endosomal and vesicular antibody markers for immunofluorescence assays. These markers will later be used in cell-based models and hypothalamic tissue from PWS patients to study how the loss of MAGEL2 affects endosomal trafficking and may contribute to endocrine dysfunction.
Comments
Advisor: Joshua D. Stafford, joshua.stafford@mst.edu