Collaborate 2 Cure
July 17, 2017

Location:

KU Clinical Research: Fairway Auditorium
4350 Shawnee Mission Parkway  Fairway, KS 66205

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Drosophila Clueless is Involved in Parkin-Dependent Mitophagy

PINK1/Parkin-mediated mitochondrial quality control (MQC) prevents damaged organelles from fusing with the healthy mitochondrial pool, facilitating mitochondrial clearance by autophagy. Drosophila clueless (clu) was previously found to interact genetically with PINK1 and parkin to regulate mitochondrial clustering.  Here we show that the evolutionarily conserved Clu protein is essential for mitochondrial homeostasis and regulates Mitofusin/Marf degradation to promote damaged mitochondrial clearance.

Speaker- Erika Geisbrecht, PhD

Dr. Geisbrecht earned her B.S. in Genetics and Microbiology from the University of Wisconsin-Madison. Her dissertation work was completed in the lab of Denise Montell at The Johns Hopkins University School of Medicine and she continued her post-doctoral training with Susan Abmayr at the Stowers Institute in Kansas City. Dr. Geisbrecht is an Associate Professor at Kansas State University. Her current research uses the genetic model Drosophila melanogaster to understand how mutations in evolutionarily conserved genes result in disease progression.

S-Nitrosylation and Mitochondrial Fission: Then and Now by Quantitative Proteomics

The pathological processes of neurodegenerative disorders, such as acute stroke and traumatic brain injury, as well as chronic Alzheimer’s and Parkinson’s diseases engender neurovascular impairment, synaptic injury and neuronal cell damage.  Reactive nitrogen/oxygen species (RNS?ROS)-related nitrosative and oxidative stress mediates normal neuronal signaling, excessive accumulation of these free radicals is linked to neuronal cell injury or death.  Emerging evidence has demonstrated that S-nitrosylation, representing covalent reaction of an nitric oxide (NO) group with a critical protein thiol, mediates the vast majority of NO signaling.  Analogous to phosphorylation and other posttranslational modifications, S-nitrosylation can regulate the biological activity of many proteins.  This presentation will discuss the studies that implicate neuropathogenic roles of S-nitrosylation in mitochondrial dysfunction, synaptic injury, and eventual neuronal loss, particularly focusing on S-nitrosylated dynamin-related protein 1 (Drp1).  Furthermore, new, unbiased proteomic approaches on quantitative detection of S-nitrosylated proteins and mapping of S-nitrosylated sites using fluorescence and isobaric labeling techniques will be discussed.

Speaker: ZeZong Gu, MD, PhD

Dr. Gu received his medical degree from Tianjin Medical University in China and his doctorate in cell biology and neuroscience from the University of Texas Medical Branch in Galveston.  He joined Dr. Stuart Lipton at the Burnham Institute for Medical Research (now the Sanford Burnham Prebys Medical Discovery Institute) in La Jolla, California, where he advanced from a postdoctoral fellow to research assistant professor, and was then recruited to MU School of Medicine setting up of the MU Center for Translational Neuroscience and supporting the Center’s neuroscience-focused core facilities.  Dr. Gu’s interests in aging and neurodegenerative diseases include ischemia and brain injury on the nitrosative/oxidative stress-mediated redox signal transduction.  In particular, he focuses on posttranslational modifications of critical cysteine residues of proteins by S-nitrosylation and their impact on protein proteolysis, aggregation, mitochondrial fragmentation, and neuronal cell death.