Research in the Grman lab focuses on understanding how ecological processes play out in restored ecosystems, especially prairies. We ask questions like: How can we increase the diversity of plants, pollinators, and soil microbes in restored prairies? How can we increase the establishment of rare prairie plants? How do

multi-mutualistic symbioses among plants and soil microbes work in restored prairies, and can we make them work better? We address these questions in both the lab and field, using short-term plant growth experiments in the lab and long- term prairie restoration experiments in field sites around Washtenaw County and southwest Michigan.

Dr. Backues is Associate Professor of Chemistry whose lab studies autophagy – a process of cellular “self-eating” that helps cells survive starvation as well as getting rid of damaged or malfunctioning subcellular components that would otherwise be toxic to the cell. In humans, autophagy is part of our defense against infections pathogens and cancer, as well as helping to prevent neurodegenerative diseases like Alzheimer’s and Parkinson’s. Autophagy is carried out by a suite of 30+ “Atg” proteins that create the autophagosome – a double-membrane vesicle that surrounds cargo in the cytoplasm (the body of the cell) and then delivers it to the vacuole/lysosome (the stomach of the cell) where it is broken down and the nutrients are recycled. The Backues lab seeks to understand how this process works by studying the functions of key Atg proteins in baker’s yeast, an easy-to-work with model system that has most of the same autophagy proteins as humans. Current projects include studying how Atg11 interacts with Atg9 to start the process of autophagosome formation, and whether the enzymes Atg10 and Atg3  control the autophagosome size or autophagosome  number.

The toll that cancer takes on society is clear; it is the second leading cause of death in the U.S. and is associated with high medical costs, not to mention the physical and emotional expense. Similarly, Alzheimer’s Disease (AD) is the sixth leading cause of death, slowly stripping away memories and the personality of those afflicted with it, with obvious negative impacts on families and friends. Our group is currently exploring the relationship between cancer and Alzheimer’s Disease, since the likelihood of developing one appears to be inversely related to developing the other. While some of this may be age-related (patients with cancer may not survive long enough to develop AD, which more commonly afflicts the older population), it is possible that AD patients may possess some characteristic that is protective against cancer.  There are many neurotransmitters, signaling factors, and proteins involved in each disease, and some are involved in both. A common characteristic of Alzheimer’s Disease patients is formation of aggregates or plaques of the protein called  amyloid in the brain. The goal of this project is to synthesize smaller fragments of amyloid and test their effects on A549 lung cancer cells to determine whether they kill these tumor cells. This can help us narrow down what part of amyloid is necessary, which may later be developed into a treatment.

This summer, high school students will have the opportunity to dive into real-world biological research by exploring soil bacteria that potentially produce antibiotics. This project will introduce students to essential microbiology techniques as they search for bacteria in our local soil samples that can combat the antibiotic crisis the world is currently facing. This three-week experience is more than just a lab project—it’s a hands-on introduction to the world of scientific discovery, allowing students to contribute to ongoing microbiology research while developing valuable skills in microbiology and biotechnology!

Nicotine is a highly addictive component in cigarette smoke. It is known to facilitate tumorigenesis and the accelerated development of non-small cell lung cancer (NSCLC), which is known to account for ~80% of all lung cancer cases.  Our research examines, in part, how nicotine treatment of NSCLC cells regulates vascular endothelial growth factor (VEGF) signaling, known to be important in the progression of vascular disease and cancer through increased levels of the stress neurotransmitters, norepinephrine/noradrenaline, and epinephrine/adrenaline. We also examine how nicotine-induced activation of VEGF promotes the function of proteins involved in increased cell survival and suppresses the function of tumor suppressors. This work expands our scientific knowledge of mechanisms employed by nicotine in regulating VEGF signaling and also provides significant insights into novel future therapeutic strategies to combat lung cancer.