Spring 2017 Seminar Schedule

Lunch at 12 PM (University Center)/Seminar at 3 PM (Grote 411, Presentation 3-3:45 PM & Question Sesssion 3:45-4:00 PM)





January 20 Hong Qin, UTC Computer Science  Applying network theories in biology: From systems biology to precision medicine
February 3 Eric T. Lane, UTC-Retired The Chemistry of the Brain: Why is the grass always greener on the other side of the fence?
February 10 Emily Weinert, Emory University  Investigating Bacterial Signaling Proteins and Pathways: from O2-Sensing Heme Proteins to Atypical Cyclic Nucleotides
February 24 Chris Baker, UTK Micro- and nanotechnologies for “listening in” on cell-to-cell communications
March 10 Donald Burden, MTSU

“Inhibition of Human DNA Topoisomerase IIa by Gossypol”



Hong Qin, UTC Computer Science: "Applying network theories in biology: From systems biology to precision medicine"
Many challenges in biology and medicine as caused by complex networks. I will present my own network research in systems biology, genomics, and precision medicine. One focus of my research is cellular aging, and I will show how probabilistic gene network models can be used to infer gene network changes during the aging process. I will also discuss ongoing research projects in my group using network approach to tackle problems in genomics and precision medicine.


Eric Lane, UTC-Retired: "The Chemistry of the Brain: Why is the grass always greener on the other side of the fence?"

Have you ever wondered why this greener perception happens? What is the chemistry of the brain that causes it? Where did it come from? Why should we be interested in it? How pervasive is it in everyday life? Why is it useful? How can we detect when it happens to us? What can we do about it? How is it used against us? What can we do to reduce its use against us? How can we use it to our advantage? What are other implications of this mechanism in the brain?  Lots of questions to be explored, expounded on, explained, and answered.

Eric T. Lane, Emeritus Professor of Physics at UTC, graduated with a PH.D. in Theoretical Physics from Rice University. He taught physics, science, and computers at UTC from 1967 to 2004. Always interested in innovation in teaching and learning, in 1985, he won two awards for microcomputer animation in teaching. After retirement, he began research to understand how we learn, based on how the brain works. This study has, among other things, lead to the development of a procedure that relieves the symptoms of post traumatic stress for veterans and others.



Emily Weinert, Emory University: "Investigating Bacterial Signaling Proteins and Pathways: from O2-Sensing Heme Proteins to Atypical Cyclic Nucleotides"

Bacteria must sense and respond to their environment by modulating signaling pathways and phenotypes to maximize survival. Heme proteins play roles in sensing the bacterial environment and controlling the switch between motile and sessile (biofilm) states. Globin coupled sensors are heme proteins that consist of a globin domain linked by a central domain to an output domain, such as diguanylate cyclase domains that synthesize c-di-GMP, a major regulator of biofilm formation. Characterization of globin coupled sensor proteins has elucidated the effects of heme ligand binding on catalysis and protein oligomerization, as well as the downstream effects on bacterial phenotypes, such as virulence and biofilm formation. Given that bacteria form biofilms in response to numerous signals and that biofilms are linked to bacterial infections, it is important to understand the myriad small molecules and pathways controlling biofilm formation. Additional nucleotides, 2’,3’-cyclic nucleotide monophosphates, have been identified as products of mRNA degradation that are involved in modulating biofilm formation and motility. The enzyme responsible for 2’,3’-cNMP production has been identified and current studies are identifying other proteins involved in 2’,3’-cNMP metabolism and sensing. Taken together, our work provides insight into new proteins and small molecules involved in biofilm formation and motility, as well as highlights new bacterial signaling pathways.


 Chris Baker, UTK: "Micro- and nanotechnologies for “listening in” on cell-to-cell communications"

Understanding a complex biological system requires not only understanding its parts, but also understanding how those parts interact to respond to stimuli and share information. The ability for cells, tissues, and organs to communicate via chemical signals is a key differentiator that separates complex multicellular life from single celled organisms. Hormones are the chemical signals that cells use to communicate, and listening in on cell-to-cell communication requires high precision, high accuracy measurements of these hormones within complex biological samples. A broad range of chemical species act as hormones in human biology, of which peptides present one of the most analytically challenging chemical classes. The Baker Bioanalysis Lab at The University of Tennessee is developing new micro- and nanotechnologies for measuring peptide hormones that may be involved in the pathophysiology of neurodevelopment and neurodegerative diseases like autism spectrum disorder and Alzheimer’s disease. This talk will cover technology development in our research program towards biosensor platforms based on synthetic mimics of the cellular membrane. These technologies aim to measure peptide hormones via their native interactions with cell surface receptor proteins, mimicking biological signal transduction mechanisms. Related areas of research in our group will also be discussed, including microfluidic instrumentation for automated chemical separations and mass spectrometry of nL - pL sample volumes.


Donald Burden, MTSU: “Inhibition of Human DNA Topoisomerase IIa by Gossypol”

Cancers are a major public health threat worldwide, with over 1/3 of all people expected to be diagnosed with a cancer at some point in their life.  Chemotherapy is commonly used to treat cancers, and the chemotherapeutic agents are often administered as combinations of drugs.  Many chemotherapy drugs kill cells by inducing apoptosis.  One class of chemotherapeutic drugs is the topoisomerase II (topo II) poisons, a structurally diverse group of compounds that act by stabilizing a transient intermediate in the catalytic cycle of the enzyme.  Stabilizing this intermediate leads to the conversion of transient double-strand breaks in DNA into permanent double-strand breaks, and this triggers apoptosis.  There are also compounds that are topo II inhibitors rather than poisons, and these compounds inhibit the overall catalytic activity of the enzyme (altering DNA topology) without necessarily affecting the stability of the intermediate containing the transient DNA double-strand breaks.  While topo II inhibitors are cytotoxic, they have not been shown to be efficacious in treating human cancers.  These catalytic inhibitors can act by affecting one or more steps of the catalytic cycle of the enzyme.

Gossypol, a toxin from cotton plants, has been shown to be a catalytic inhibitor of topo II.  Gossypol is also known to stimulate apoptosis by inhibiting the anti-apoptotic protein Bcl2.  The (-) form of gossypol is currently being studied in clinical trials under the name AT-101.  AT-101 has been used as a pro-apoptotic drug in these trials in combination with other chemotherapeutic drugs, including at least one topo II poison.  Elucidating the mechanism whereby gossypol/AT-101 inhibits the catalytic activity of topo II is necessary, as this mechanism may interfere with the ability of the enzyme to be poisoned.  If this is the case, it may impact future work on combination chemotherapy involving AT-101 and topo II poisons.  Preliminary results suggest that racemic gossypol inhibits DNA binding by topo II, and this may result in a reversal of the actions of the clinically useful topo II poisons.