Hereditary spastic paraplegia (HSP) is a group of inherited neurologic disorders that cause weakness and stiffness in the leg muscles. Defects in membrane trafficking can contribute to HSP and other neurodegenerative diseases. For her Ph.D. research, IPiB graduate student Jennifer Peotter focused on a critical protein, TFG, that’s been shown to be mutated in patients with HSP.
Peotter’s experiments, performed in a rodent model, show that TFG possesses a specialized role in membrane trafficking outside of its typical functions in the early secretory pathway (where proteins destined to extracellular spaces or to organelles are synthesized and traverse the endoplasmic reticulum). Her results also indicate how the mutation in TFG seen in patients with HSP alters critical trafficking pathways in neurons and may lead to observable changes in electrophysiology.
“Understanding the pathomechanism of my specific model contributes to the overall understanding of how highly polarized cells, such as neurons, orchestrate a diverse and complicated set of membrane trafficking needs,” says Peotter, who works in the Audhya Lab. “Not only does this improve our understanding of other neurodegenerative diseases but also further elucidates the specialized functions of the early secretory pathway.”
During her time in IPiB, one of Peotter’s goals was to learn about the business side of biotechnology. A classmate recommended that she join WiSolve Consulting Group, and Peotter was involved in that organization for three years. After defending her Ph.D. research, she will take her problem solving and data analytics skills to Boston Consulting Group, where she will be employed as a consultant.
To learn more about Peotter’s research, attend her Thesis Defense on Thursday, June 23 in Room 1211 of the DeLuca Biochemical Sciences Building.
Note: An earlier version of this post stated that Peotter’s defense was May 23. It will be held June 23.