The importance of understanding the inflammatory response in the lungs is underscored by the fact that pneumonia and influenza illnesses led to an estimated 12,000 deaths in the 2015-16 U.S. flu season. Our research investigates the expression and regulation of versican in response to lung infections, both viral and bacterial. Versican is a chondroitin sulfate proteoglycan present in the extracellular matrix; it is expressed in lungs during embryonic development, mostly absent during healthy adulthood, and re-expressed in instances of inflammatory lung injury or infection. We are interested in understanding the pathways that result in versican upregulation, as preliminary data suggest that versican can be either pro- or anti-inflammatory, depending on the type of cell it arises from. My research project investigates this differential regulation phenomenon - recently, I have incorporated chromatin immunoprecipitation (ChIP) of versican transcription in both viral-stimulated macrophages and lung fibroblasts to explore the epigenetic factors that control expression. ChIP allows us to establish and quantify interactions between proteins and DNA; in our case, we are interested in transcription factors that follow interferon beta signaling (IFNb), which has been shown by our lab to be a key mediator of versican expression. IFNb itself is a known anti-viral cytokine, suggesting that versican may also follow this response to viral infection. If we can determine which transcription factors, if any, lead to an increased response of versican, we will have identified a signaling pathway by which to manipulate versican expression. The ultimate goal of this work is to develop a lung inflammation therapy by driving production of versican in an anti-inflammatory state. Utilizing versican's power as an immunomodulatory molecule could be a new tool for fighting severe inflammation associated with respiratory illnesses.

Diet, lifestyle, and environment can influence an individual’s behavior and brain function through epigenetic mechanisms. The Lattemann lab is investigating the effect that one factor, high fat diets, has on epigenetic regulation in hippocampus a key area for learning, memory and cognition. Previously, the lab determined that rats fed high fat diets exhibited increased sucrose motivation, and this behavioral effect was later linked to stearic and palmitic fatty acids explicitly. It was also shown that high fat, high sugar diets are associated with impaired place memory in rats. Most recently, the lab has analyzed hippocampal chromatin from rats fed high stearic and palmitic acid diets and is in the process of determining the effect of these diets on histone modifications. Histones regulate gene expression by binding to DNA: modifications to these histones influence how readily the DNA is transcribed, and how the gene expressed. These modifications are being screened for using Western blot analysis. In addition to screening for modifications in histones, the Lattemann lab also directly analyzed DNA for the expression of target genes. This screening procedure included measuring expression of candidate histone-target genes using PCR, and ChIP-Seq (Chromatin Immunoprecipitation and unbiased gene screening) assays. By locating histone modifications and quantitating the expression of hippocampal candidate genes, the lab has provided an epigenetic explanation for the behavioral effect of the diets, and a possible molecular mechanism by which the diets can induce this effect.

With climate change, it is predicted that plants will experience longer periods of drought followed by sudden heavy rainfall at unpredictable intervals. Using Arabidopsis thaliana as a model plant, we want to better understand how these variable conditions will impact plant communities in face of climate change. As we experience global climate change, this research will allow us to understand how plant communities may respond evolutionarily to the changing environment. We believe selective pressure created by climate change will promote phenotypic plasticity and epigenetic “memory” of their drought experience. This "memory" is passed down through generations and may help plants cope with the environmental stress. My research is part of Undergraduate Phenotyping of Arabidopsis Knockouts (unPAK), a community that strives to better understand genotype-phenotype relationship—how the DNA of an organism influences the way genes are outwardly expressed. My research aims to understand the significance this relationship plays in the adaptive ability of plants when exposed to variable conditions. We will grow 4 generations of 5 different genotypes of A. thaliana we believe have different levels of phenotypic plasticity. Generation 0, 1 and 2 will be exposed to either drought or regular watering, and Generation 3 will receive inconsistent watering. For Generation 0, we exposed 175 plants to drought (little to no watering), and 175 to regular watering (20mL every week). While growing these plants, we collected quantitative phenotypic observations such as chlorophyll content and rosette diameter. Eventually, we will measure fitness by number of seeds produced. For each generation, we’ll extract DNA from these plants and look at methylated regions, allowing us to compare their epigenetic responses to the treatments, analyze whether their plasticity benefits them in adapting to stressful environments, and see if there’s any difference between the parent and the offspring generations at the molecular level.