Biomedical Sciences - Seminar Series

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Biomedical Sciences Seminar Series

The seminar series is a weekly scientific forum with the following goals

Maintain awareness of research within the department by providing faculty members an opportunity to disseminate professional accomplishments to their peers
Foster inter-departmental interactions and collaborations by including speakers from other departments/units on campus with shared interests
Promote the professional development of graduate students/postdocs within the department by inclusion within the series
Support professional development of faculty by inviting notable speakers from outside institutions

Location and times

Generally each Wednesday, from 12:00 – 1:00pm (see schedule below)
Room 1302 of the Biomedical Sciences Building
Note: food and drink are not allowed in the seminar room

Nominating speakers/questions regarding the series

All questions may be directed to Dr. Michael Blaber (michael.blaber@med.fsu.edu)

Fall 2009 Schedule

Dr. Jihun Lee	Wednesday, August 26th The interaction between Thermostability and Buried Free Cysteines in Regulating the Functional Half-life of Fibroblast Growth Factor-1 Postdoctoral Research Associate Florida State University Postdoctoral fellow, Florida State University (2007-present) Ph.D. Chemistry and Biochemistry, Florida State University (2007) B.A. Chemistry, Microbiology, Sunmoon University, South Korea (2001) Protein biopharmaceuticals are an important and growing area of human therapeutics; however, the intrinsic property of proteins to adopt alternative conformations (as during protein unfolding), presents numerous challenges limiting their effective application as biopharmaceuticals. Using fibroblast growth factor-1 (FGF-1) as a model system, we describe a cooperative interaction between the intrinsic property of thermostability and the reactivity of buried free cysteine residues that can substantially modulate protein functional half-life. A mutational strategy is described that combines the elimination of buried free cysteines with secondary mutations that enhance thermostability to achieve a substantial gain in functional half-life. Furthermore, the implementation of this design strategy utilizing stabilizing mutations within the core region resulted in a mutant protein that is essentially indistinguishable from wild-type as regards the protein surface and solvent structure; thus, minimizing the immunogenic potential of the mutations. The design strategy should be generally-applicable to soluble globular proteins containing buried free cysteine residues.

Dr. Myra Hurt	Wednesday, September 2nd Phosphorylation of the Transcription Factor YY1 Professor of Biomedical Sciences Senior Associate Dean for Research and Graduate Programs, FSU College of Medicine. Associate dean for student affairs, admissions and outreach, FSU College of Medicine (2001-2004). Acting dean, FSU College of Medicine (2000 to 2001). Director of Program in Medical Sciences, FSU. Associate professor of Biological Science, FSU. Assistant professor of Biological Science, FSU. Postdoctoral Fellow, Cell and Molecular Biology, Baylor College of Medicine, Houston, Texas. Ph.D., Microbiology, University of Tennessee Center for the Health Sciences, Memphis, Tenn. B.S., Biology, Henderson State University, Arkadelphia, Ark. YY1 is a multifunctional transcription factor that has been shown over the past decade to be involved in almost all aspects of cellular life and death. Through the control of a large array of genes, YY1 has been shown to regulate development, growth, differentiation, cell cycle, DNA repair, and even apoptosis. We have previously established a link between YY1 and histone gene regulation at G1/S stage of the cell cycle. However, the upstream pathways regulating YY1 are still enigmatic. We have explored the regulation of YY1 through phosphorylation pathways. We have uncovered a mechanism for the inactivation of YY1 in mitosis through the phosphorylation of its DNA binding domain. We have identified several kinases that phosphorylate YY1 in vitro and mapped their target sites. Through the generation of phospho-specific antibodies for these sites, we are currently exploring their functions in vivo. Upregulation of YY1 in certain cancers and its ability to suppress cellular responses to some apoptotic stimuli makes it a potential target for therapeutic treatments, based on a better understanding of its regulation.

Dr. Scott Stagg	Wednesday, September 9th The Structures of COPII Coats and Tubes Assistant Professor Chemistry and Biochemistry Florida State University Postdoctoral Fellow, The Scripps Research Institute (2004-2007) Postdoctoral Fellow, Georgia Institute of Technology (2003) Ph.D. University of Alabama at Birmingham (2002) B.S. Biology, Oglethorpe University (1996) COPII vesicles are responsible for packaging and transporting over 10,000 different cargo molecules (about one-third of the eukaryotic genome) of widely varying sizes and shapes from the endoplasmic reticulum (ER) to downstream compartments of the secretory pathway. We previously solved two different COPII structures that showed: 1) that the COPII protein Sec13/31 may form cages of increasing size based on the simple rule that the geometry of the cage is dictated by four Sec13/31 heterotetramers combining to form a vertex, 2) possible mechanisms for the coordination of cargo collection and coat assembly, and 3) mechanisms for the collection of cargo of varying size. We recently discovered that Sec13/31 will form a tubular structure at high concentrations. Cryogenic electron tomography was used to determine the structure of these COPII tubes. This showed that the tubes are formed by the concatenation of Sec13/31 cages. where the vertices of one cage are located in the triangular faces of its neighbors. This gives rise to a hollow tube with an inner diameter of 300Å. We speculate that these tubular structures are important for transporting elongated cargo such as procollagen in the cell.

Dr. Anant K. Paravastu	Wednesday, September 16th Solid state NMR structural investigations b-amyloid fibrils and designer self-assembled protein nanofibers Assistant Professor of Chemical and Biomedical Engineering Florida State University Assistant Professor of Chemical and Biomedical Engineering, FSU (2008) Postdoctoral fellow, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Helath (2004-2008) Ph.D., Chemical Engineering, University of California Berkeley (2004) B.S., Chemical Engineering, Massachusetts Institute of Technology (1998) Protein self-assembly is interesting because of its role in “protein misfolding” diseases and in the formation of extracellular matrices. I will present solid state NMR-derived structural data on Alzheimer’s -amyloid fibrils that demonstrate structural polymorphism and environment-dependent molecular structure. These results may explain certain disease-related observations, such as the phenomenon of strains in prion diseases. I will subsequently describe preliminary studies of designer self-assembling protein systems that form amyloid-like structures. With sufficient control of self-assembly, designer proteins could make important contributions to the field of regenerative medicine.

Dr. Branko Stefanovic	Wednesday, September 23rd Type I collagen and fibrosis; regulation of expression and finding a cure Associate Professor of Biomedical Sciences Florida State University Associate Professor, College of Medicine, FSU Assistant Professor, College of Medicine, FSU Research Assistant Professor, UNC Chapel Hill Postdoctoral fellow, University of Bern Ph.D., FSU Type I collagen is the most abundant protein in human body. It is expressed in bone, tendon and skin, however, its ectopic expression in the parenchymal organs results in fibroproliferative disorders (fibrosis). 45% of deaths in the USA had an underlying fibroproliferative disorder. There is no cure for fibrosis and understanding regulation of expression of type I collagen is necessary to find an effective antifibrotic drug. This seminar will address the novel aspects of regulation of type I collagen discovered in my lab. It will also present the first attempts to manipulate its expression, as the beginning to find a cure for one of the major causes of morbidity and mortality in the USA.

Dr. Debra Ann Fadool	Wednesday, September 30th Insulin Modulation of Kv1.3 Channel Function in Obesity – My Sabbatical Research Associate Professor, Program In Neuroscience & Molecular Biophysics Florida State University Associate Professor of Biology, FSU (2004- present) Assistant Professor of Biology, FSU (1999-2004) Postdoctoral fellow, Biochemistry, Brandeis University (1994- 1996) Ph.D. Zoology, Whitney Laboratory, UF (1993) M.Sc. Analytical Chemistry, University of Rhode Island (1987) B.Sc. Biology & English, Albion College, Michigan (1985) We have recently discovered that a member of the voltage-gated potassium ion channel, Kv1.3, is a molecular target for tyrosine kinase signaling cascades including insulin. Gene-targeted deletion of the channel elicits a spectrum of phenotypes that includes a resistance to diet- and genetically-induced obesity, a “super-smeller” ability in terms of odor discrimination and threshold, changes in axonal targeting to the olfactory bulb, alteration of the expression of protein scaffolds, and differential pruning of olfactory sensory neurons. We developed an intranasal delivery method to introduce insulin across the blood brain barrier to reach the Kv1.3 targets of the olfactory bulb. In my presentation I will describe my sabbatical leave research project where I made slice electrophysiological recordings of obese and intransal insulin treated mice to understand the chronic state of channel modulation while under an altered metabolic state.

Hyeong-Min Lee	Wednesday, October 7th Essential roles of CKIδ and CKIε in the mammalian circadian clock Graduate student of Biomedical Sciences Florida State University Graduate student of Biomedical Sciences, FSU (2006~present) M.S. Korea University (2000) Circadian rhythms in mammals are generated by a negative transcriptional feedback loop in which PERIOD (PER) is rate-limiting for feedback inhibition. Casein Kinase Ie and Id (CKIe/d) can regulate temporal abundance/activity of PER by phosphorylation-mediated degradation and cellular re-localization. Despite their potentially crucial effects on PER, it has not been demonstrated in vivo that these kinases play essential roles in circadian rhythm generation as does their homolog in Drosophila. In this presentation I will present molecular evidence that CKIe/d are essential for the mammalian circadian clock.

Dr. Gregory Dudley	Wednesday, October 14th Organic synthesis and methodology inspired by natural products: C-C bond cleavage Associate Professor of Chemistry and Biochemistry Florida State University Associate Professor of Chemistry and Biochem, FSU (2008) Assistant Professor of Chemistry and Biochem, FSU (2002) NIH Postdoctoral fellow, Memorial Sloan–Kettering (2000-2002) Ph.D. Massachusetts Institute of Technology (2000) B.A. Chemistry, Florida State University (1995) Research in the Dudley Lab is designed to further the science and practice of organic chemistry in order to advance the drug discovery process. Individual projects are synthesis-driven, with natural products serving as an inspiration for new methods. The presentation will focus on the development of new organic reactions and will include discussion of other important problems in synthetic organic chemistry.

Dr. Yanchang Wang	Wednesday, October 21st The role of mitotic exit pathways in spindle elongation Associate Professor of Biomedical Sciences Florida State University Associate Professor of Biomedical Sciences, FSU (2009) Assistant Professor of Biomedical Sciences, FSU (2003) Postdoctoral fellow, Baylor College of Medicine (1997-2002) Ph.D. University of Virginia (1993-1997) MSc, Peking Union Medical College (1986-1989) B.A. Microbiology and Chemistry, Hebei University (1984) Protein phosphorylation is one of the important ways to regulate protein activity and cyclin-dependent kinases (CDK) phosphorylate hundreds of proteins to control cell cycle progression. Accumulating evidence indicates the important role of dephosphorylation of these CDK substrates in cell cycle progression. In budding yeast, two mitotic exit pathways, FEAR and MEN, control the timing of the dephosphorylation of CDK substrates by activating a protein phosphatase Cdc14. Here, we present evidence that M-phase cyclins promotes the formation of binucleate cells due to premature spindle elongation. Interestingly, this effect depends on the FEAR pathway, which activates the phosphatase Cdc14 during early anaphase to dephosphorylate S-phase cyclin substrates and facilitate spindle elongation.

Dr. Wu-Min Deng	Wednesday, October 28th Developmental regulation of cell proliferation in Drosophila Associate Professor of Biological Sciences Florida State University Associate Professor of Biological Science, FSU (2009) Assistant Professor of Biological Science, FSU (2003) Postdoctoral fellow, University of Washington (1998-2003) Ph.D. The University of Edinburgh (1997) M.Sc. Shanghai Inst. Of Cell Biology (1994) B.Sc.. Genetics, Sichuan University (1991) Coordinated regulation of cell proliferation and differentiation in strict temporal and spatial patterns is fundamental to the development of multicellular organisms. We use the Drosophila epithelial cells as a model system to understand how cell proliferation is regulated in development. For example, we are interested in how cells leave the mitotic cycle and enter endoreplication cycle to stop proliferation. What are the developmental signals that regulate the change of cell cycle status? We are also interested in the molecular mechanisms underlying cell competition, during which cells undergo compensatory proliferation.

Dr. Qin Wang	Wednesday, November 4th Regulation of GPCR function by Spinophilin Assistant Professor of Physiology and Biophysics University of Alabama at Birmingham Assistant Professor of Physiology and Biophysics, UAB (2005) Assistant Professor of Neurobiology, UAB (2006) Research Assistant Professor, Vanderbilt University (2002-2005) Postdoctoral Fellow, Vanderbilt University (2000-2002) PhD, University of Iowa (1999) MD, Beijing Medical University (1992) Non-G protein-interacting partners appear to play pivotal roles in modulating nearly every aspect of GPCR activity (trafficking, signaling and pharmacology). We have identified spinophilin as an interacting partner for the alpha2 adrenergic receptor (AR), a subfamily of GPCRs. Spinophilin interaction with the alpha2-AR causes profound consequences on receptor trafficking, signaling and in vivo response extent and sensitivity. Furthermore, spinophilin-alpha2-AR interaction is modulated by PKA phosphorylation of spinophilin, representing a potential mechanism for cross-regulation of the alpha2-AR by other mechanisms.

Samantha Zeitlin, Ph.D.	Wednesday, November 11th Making a break for it: DNA damage creates a binding site for centromere proteins Postdoctoral Fellow Ludwig Institute for Cancer Research University of California, San Diego Postdoctoral fellow with Don Cleveland (CIRM fellow) Postdoctoral fellow with Jean Wang (NIH F32-03) Postdoctoral fellow with John Newport (NIH F32) Ph.D. Molecular and Cellular Structure and Chemistry, The Scripps Research Institute (2002) B.A. Biochemistry, University of Pennsylvania (1997) Inheritance in eukaryotes is not only dictated by the genetics of DNA, but also by the epigenetics of chromatin proteins that wrap the DNA. The centromere is the site of mitotic spindle attachment to chromosomes, and it is thought to be specified by an epigenetic mechanism. Specifically, the pattern of the epigenetic marker histone H3 variant, Centromere Protein A (CENP-A), is inherited. The mechanism of initial CENP-A recruitment has been a longstanding question in the field. In this presentation I will present experimental evidence that CENP-A is recruited by DNA damage, and propose a testable model for centromere specification and maintenance by this mechanism.

Dr. Michael Roper	Wednesday, November 18th Microfluidic systems for measuring intracellular Ca2+ and secretion dynamics from islets of Langerhans Assistant Professor of Chemistry and Biochemistry Florida State University Assistant Professor of Chemistry and Biochemistry, FSU (2006) Postdoctoral fellow, University of Virginia (2003-2006) Ph.D. University of Florida (2003) B.S. Chemistry, University of Texas at Austin (1998) Microfluidic devices are platforms that contain micron-sized channels produced via photolithography. We use these devices to both control and sample the extracellular environment around biological cells in a highly automated and highly sensitive manner. In this presentation, recent results will be shown when intracellular Ca2+ dynamics in single mouse islets of Langerhans were monitored upon stimulation with gradients of glucose concentration that mimicked in vivo glucose oscillations. Simultaneous measurement of insulin and glucagon secretion will also be shown using a two-color electrophoretic immunoassay with a temporal resolution of 10 seconds, allowing the secretory dynamics of islets to be observed.

Lori L. Wallrath	Wednesday, December 2nd Heterochromatin Protein 1: Linking Drosophila gene silencing and human breast cancer progression Professor of Biochemistry University of Iowa Professor of Biochemistry, University of Iowa (2009) Associate Professor of Biochemistry, University of Iowa (2003) Assistant Professor of Biochemistry, University of Iowa (1997) Postdoctoral Fellow, Washington University in St. Louis (1991-1996) Ph.D. Genetics, Michigan State University (1991) B.A. Microbiology, Michigan State University (1986) Post-translational modifications of histones serve as epigenetic marks that control transcription, DNA repair and other chromosomal processes. In some cases these marks function as binding sites for non-histone chromosomal proteins. An example is histone H3 lysine 9 methylation, a modification that is specifically recognized by Heterochromatin Protein 1 (HP1). We are using the genetic and genomic tools available in Drosophila to understand the mechanism by which HP1 spreads along the chromatin fiber and silences gene expression. Our studies have implications for understanding changes in gene expression associated with breast cancer progression. We have discovered that HP1 regulates the invasive potential of human breast cancer cells. A model that connects HP1 to cell signaling involved in breast cancer metastasis will be presented.

Dr. Lisa C. Lyons	Wednesday, December 9th Circadian Modulation of Memory in Aplysia Assistant Professor, Dept. of Biological Science, Program in Neuroscience Florida State University Research Assistant Professor, University of Houston (2004- 2007) Postdoctoral fellow, University of Houston (2000-2004) Ph.D. University of Houston (2000) M.S. Biology, Lamar University (1991) B.S. Bioenvironmental Science, Texas A&M University (1988) Identification of the processes through which memory may be modulated is a fundamental component in unraveling the mechanisms through which learning and memory occur. The marine mollusk Aplysia californica has long proven a superb model for studies of learning, with extensive research by many scientists contributing to our understanding of the molecular and cellular mechanisms involved in memory formation. We have used Aplysia to investigate how the endogenous circadian clock modulates learning and the formation of memory in vivo. Previously, we found that the circadian clock strongly modulates long-term, but not short-term, memory formation for non-associative sensitization and the associative paradigm, learning that food is inedible (LFI; Fernandez et al., 2003; Lyons et al., 2005). Recently, we found that the circadian clock also modulates non-associative intermediate-term sensitization (Lyons et al., 2008) and associative LFI memory. Based on our studies, we predict that robust circadian modulation of long-term and intermediate-term memory results from circadian modulation of multiple steps during the induction and formation of memory, in particular, highly conserved processes.

Dr. Hong Li	Wednesday, January 20th Making Ribosomes and Spliceosomes: Structural Perspectives Associate Professor of Chemistry and Biochemistry Florida State University Associate Professor of Chemistry & Biochemistry, FSU (2006) Assistant Professor of Chemistry & Biochemistry, FSU (1999) Postdoctoral fellow, Caltech (1996-1999) Postdoctoral fellow, Brookhaven National Laboratory (1992-1994) Ph.D. University of Rochester (1992) B.A. Physics, Sichuan, P.R. China (1983) Ribosomes and spliceosomes are made up of multiple RNA and protein subunits. These large ribonucleoprotein particle machines are maturated through a series of elaborative processes that include site-specific cleavage and modification of their RNA components. Three dimensional structures of the modifying enzymes now provide atomic views of the maturation process and reveal mechanisms for overcoming topological and chemical challenges in capturing and modification of large RNA substrates.