The Department of Biology Fall Seminar Series is hosted on Fridays at 4 p.m. in CN 160, located in the center of the Cooper Science Building on the southwest end of campus. All lectures are free and open to the public with no registration required.

September 8

Dr. Catherine A. Wakeman, Texas Tech University, Biological Sciences, guest of Dr. John McKillip

"Co-infection and co-evolution during chronic infection"
Sites of chronic infection, such as the cystic fibrosis lung and diabetic foot ulcers, contain numerous pathogenic species that must co-evolve in the face of the host immune system. Commonly-isolated pathogens, such as Pseudomonas aeruginosa and Staphylococcus aureus, have been shown to evolve unique strategies to cope with this harsh environment. My research explores the hypothesis that prolonged evolution in these infectious sites selects for cooperation between these two classically competing microbes, enabling both microorganisms to exploit each other's unique survival mechanisms.

September 22

Dr. Karen Litwa, East Carolina University, Brody School of Medicine, Anatomy & Cell Biology, guest of Dr. VJ Rubenstein

“Mini-Brains on the Mind: Modeling the Molecular Mechanisms of Autism”
The development of human brain circuitry integrates neuronal differentiation, migration, and neurite extension to ultimately form trillions of synapses. Synapse development is disrupted in Autism, where elevated levels of excitatory synapses are observed in both post-mortem patient samples and mouse models. Identifying molecular mechanisms for this increased excitatory synapse formation is essential for developing Autism therapies. Yet, scientists previously lacked the ability to observe the development human brain circuitry and the prenatal emergence of Autism pathology. However, brain cortical organoids from patient induced pluripotent stem cells provide an unprecedented opportunity for us to model the formation of these neuronal connections and the alterations that underlie Autism synaptic pathology. These Autism-derived organoids exhibit increased excitatory synapse formation. Our exciting preliminary evidence indicates that elevated Rac1-driven actin polymerization drives excitatory synapse formation in early cortical development. Rac1 activity regulation is an attractive therapy since Rac1 critically regulates numerous processes underlying Autism pathology, such as cellular differentiation and nervous system development. Our current research efforts are focused on identifying Rac1 regulators specific for excitatory synapse development for more precise therapeutic intervention.

October 13

Dr. Jordan M. Marshall, Indiana University-Purdue University Fort Wayne, IN, Department of Biology, guest of Dr. Kemuel Badger

"Interacting Layers Defining Pest Status: Understanding Emerald Ash Borer Behavior, Preferences, and Host Survival"
Emerald ash borer is a pest in North American ash species and its behavior is important to detection and management. Host selection behavior and feeding preferences have direct implications regarding ash survival in North American forests. By understanding the defining variables of pest status, we can improve the likelihood of retaining ash and managing emerald ash borer.

October 27

Dr. Heather A. Hundley, Indiana University, biochemistry and molecular biology, Medical Sciences Program, guest of Dr. Douglas Bernstein

"The identification of RNA 'edits' essential for proper neuronal function"
DNA is the same in all cells of an organism, but specific cell types need to perform distinct functions at different points during development. Therefore, animals have developed ways to produce proteins with unique functions. One of these is through a process called RNA editing, in which the letters in RNA are changed in specific cells and at certain points in development. Over 60% of human transcripts contain adenosine (A) to inosine (I) “edits” that are catalyzed by the ADAR family of RNA binding proteins. ADARs serve an essential physiological role by converting specific adenosines to inosines within codons and thus expanding the proteome. In addition, ADARs can alter specific adenosines in introns and untranslated regions to alter splicing and small RNA binding, thereby regulating gene expression. As loss of ADARs affects neuronal function in all animals studied to date, one of the primary biological functions of ADARs is to promote proper neuronal function. However, exactly which transcripts require RNA editing to allow an organism to exhibit normal neuronal function are unknown. By combining a cutting-edge approach to isolate neural cells from Caenorhabditis elegans (nematode worms) with RNA sequencing, we recently identified a gene that undergoes RNA editing, is mis-expressed in worms lacking RNA editing and, when transgenically expressed, can restore proper neuronal function to worms that lack RNA editing.

November 10

Dr. Adam Berland, Ball State University, Department of Geography, guest of Dr. Kemuel Badger

"Where are the urban trees and why does it matter?"
Trees are a key component of the urban environmental landscape, and we rely on trees to provide a range of ecostystem services such as stormwater control, aesthetics, and increased property values. While we are only beginning to generate reliable estimates of these ecosystem services, it is clear that these benefits are substantial in magnitude, dependent on local context, and they change other time in response to biophysical and anthropogenic drivers. In many cities, a lower abundance of trees in underserved neighborhoods signals potential environmental injustice because these neighborhoods have reduced access to ecosystem services provided by trees. I will discuss environmental justice perspectives from my research by considering the causes and consequences of uneven tree distributions within our cities. For example, Indianapolis has seen an impressive increase in street trees since 2003, but these trees have not been evenly distributed with respect to race or educational attainment. On the other hand, a different pattern is emerging in the shrinking city of Toledo, Ohio, suggesting that we need to pay more attention to the nuances of quantifying urban tree cover.

December 1

Dr. Philip Smaldino, Ball State University, Department of Biology

"A tangLed MesS: Untying DNA and RNA ‘knots’ in a deadly neurodegenerative disease”
Our group investigates a fatal neurodegenerative disease for which there is no cure. Specifically, I will discuss our work studying the role of a human helicase, G4 Resolvase1, in amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease. A subset of ALS is caused by an expansion of a (GGGGCC)n repeat in the gene, C9ORF72 (C9 ALS). Healthy individuals harbor between 2 and 30 repeats, while C9 ALS patients have >30 and often harbor 1000’s of these repeats. The expanded C9 repeat is prone to fold into complex, extensive structures termed G-quadruplexes. Excess of C9 G-quadruplex structures leads to an accumulation of abnormal RNA and protein species within a cell. The net effect of these aberrations is neuronal death and subsequent ALS pathology. Therefore, C9 ALS can be thought of as a ‘G-quadruplex disease’. We are particularly interested in this observation due to the focus of our lab on the human enzyme, G4 Resolvase1, which is proficient at untying G-quadruplex structures. I will discuss direct connections and novel functional roles for this enzyme in C9 ALS.