Dr. Brad Day received his Ph.D. from the University of Tennessee in Microbiology in 1999 where his research focus was biochemical characterization of Nod signal perception in soybean. In 2000, he received a co-sponsored National Science Foundation (U.S.) and Science and Technology Agency (Japan) postdoctoral fellowship. From 2000-2002, he conducted research at the National Institute of Agrobiological Sciences in Tsukuba, Japan, where his research contributed to the early understanding of the molecular-genetic signaling events associated with immune activation following chitin perception in rice. In 2002, he moved to U.C. Berkeley where he was a NIH Ruth L. Kirschstein Postdoctoral Fellow in the laboratory of Brian Staskawicz. As an NIH-funded postdoc at Berkeley (2002-2006), he expanded his research interests to focus on the molecular-genetic basis of host immunity, using the Arabidopsis-Pseudomonas interaction as a disease model. During this time, his research contributed to establishing what is now commonly referred to as the Guard Hypothesis. In 2006, he accepted a position at Michigan State University as an Assistant Professor. Since 2006, his lab at MSU has worked to define the role of the actin cytoskeleton as a signaling platform for immune signaling in plants, and in this area, his group was the first to identify a link between the function of the actin cytoskeleton and gene-for-gene resistance. In parallel to these studies, research in the Day lab has also published extensively in the area of immune signaling in cucumber, and more recently, has expanded into the area of DNA-nanosensor technology for the detection of pathogens. Dr. Day serves as the Associate Chair for Research in the Department of Plant, Soil and Microbial Sciences. In 2017, Dr. Day was promoted to the rank of Professor.
The laboratory of Dr. Brad Day at Michigan State University focuses on the molecular-genetic and biochemical processes associated with the interaction between plants and pathogens. Specifically, we are interested in how plants protect themselves from pathogen infection using both preformed and induced defense responses. Using a combination of cell biology and genetics, we are investigating how the actin cytoskeleton impacts defense signaling in the model system Arabidopsis thaliana. We are also using genetics and biochemistry to ask how resistance signaling is initiated during the early stages of the host-pathogen association through the function of the host actin cytoskeleton. For example, our recent work has identified a suite of Pseudomonas syringae type III effector (T3E) proteins that specifically target the Arabidopsis actin cytoskeleton. We are now working to define 1) the basal function of these specific effector targets/processes, and 2) the impact of pathogen targeting on the disruption of homeostatic cellular processes requiring actin. Our ultimate goal is to not only use pathogen T3Es as molecular and cellular probes to better define immune signaling, but to use these effectors to interrogate the function and regulation of these processes in the absence of pathogen infection.