September 25, 2018
Erika Geisbrecht featured speaker for Biochemistry and Molecular Biophysics Seminar Sept. 26
Submitted by Biochemistry and Molecular Biophysics
Erika Geisbrecht, associate professor of biochemistry and molecular biophysics in K-State's College of Arts and Sciences, is the featured speaker for Biochemistry and Molecular Biophysics Seminar at 4 p.m. Sept. 26 in 120 Ackert Hall. She will present "Through thick and thin: The path toward muscle proteostasis."
Geisbrecht earned her doctorate under Denise Montell at Johns Hopkins School of Medicine. She continued with a National Institutes of Health NRSA Postdoctoral Fellowship in Susan Abmayr's lab at the Stowers Institute for Medical Research. She moved into directing her own research as an assistant professor at the University of Missouri, Kansas City before joining the faculty in biochemistry and molecular biophysics at K-State. The Geisbrecht lab specializes in studying the mechanisms that underlie muscle structure and function. They seek to characterize molecules and signaling pathways in the Drosophila model that regulate the formation and stability of muscle-tendon interfaces; and maintenance of mature, contractile myofibers. We feel that understanding the molecular events that contribute to the development and homeostasis of normal muscle tissue will allow us to ultimately determine how defects may lead to the onset and progression of human myopathies.
Presentation abstract: The inability to maintain proteostasis in non-dividing cells such as neurons or muscles is a key factor in the development and progression of neurodegenerative diseases and myopathies. It is also a hallmark of aging cells. Autophagic signaling pathways and the ubiquitin proteasome system are two major degradative routes for protein disposal that when disrupted, result in a loss of muscle function and eventual cell death. The syncytial muscles in the fruit fly Drosophila melanogaster are an exemplary model to understand the cellular and molecular events that balance the synthesis and degradation of proteins. Inherent advantages include the structural and functional conservation of proteins and signaling pathways, less redundancy compared to mammalian models, and a genetically amenable platform to rapidly assess morphological changes in muscle structure and function. Genetic approaches have uncovered mutations in two genes that give rise to dystrophic muscle. Each of these genes is required for different aspects of proteostasis, such as maintaining glycolytic flux to supply metabolic intermediates for protein synthesis or in regulating protein turnover to prevent protein aggregation. Recent and future work on both of these projects will be presented.