{"id":105906,"date":"2025-02-04T11:19:08","date_gmt":"2025-02-04T17:19:08","guid":{"rendered":"https:\/\/engineering.wisc.edu\/?post_type=tribe_events&p=105906"},"modified":"2025-02-17T13:44:05","modified_gmt":"2025-02-17T19:44:05","slug":"bme-seminar-series-mehmet-orman-phd","status":"publish","type":"tribe_events","link":"https:\/\/engineering.wisc.edu\/event\/bme-seminar-series-mehmet-orman-phd\/","title":{"rendered":"BME Seminar Series: Mehmet Orman, PhD"},"content":{"rendered":"
Mehmet A Orman, PhD Abstract: In this talk, I will highlight our strategies to study and target persister cell metabolism in bacteria and cancer. Contrary to the belief that persister cells in bacteria have suppressed metabolism, we show that their survival depends on energy metabolism, particularly oxidative phosphorylation. In bacteria, the cyclic-adenosine monophosphate and its receptor protein redirects metabolism from anabolism to oxidative phosphorylation, highlighting the importance of the tricarboxylic acid cycle, electron transport chain, and ATP synthase. Similarly, in melanoma persisters, chemotherapy-induced stress increases mitochondrial activity, revealing a dual role of treatment\u2014inducing apoptosis in most cells while promoting a dormant, drug-tolerant subpopulation. Understanding these metabolic adaptations opens new avenues for therapeutic interventions, aiming to eradicate persister cells and prevent disease recurrence.<\/p>\n\n\n\n
Associate Professor
Chemical and Biomolecular Engineering Department
University of Houston<\/strong><\/p>\n\n\n\n
My research focuses on understanding drug-tolerant phenotypes, particularly persister cells, in both prokaryotic and eukaryotic systems. Persister cells are temporarily tolerant to drugs and contribute significantly to disease recurrence. We investigate their molecular makeup, including metabolite profiles, RNA expression, protein composition, and regulatory networks, to identify key survival mechanisms and potential therapeutic targets. Our ongoing projects include investigating self-digestion-mediated tolerance in bacterial persisters, host-pathogen interactions in drug tolerance, metabolic and repair pathways in bacterial and cancer persisters, and the immunomodulatory potential of microbial cells to harness host-pathogen interactions for cancer therapy.<\/p>\n\n\n\n