The Department of Molecular Microbiology and Immunology's (MMI) mission is to maintain active and integrated research programs that study the interactions between microbes and their hosts. The goal is to understand how these influence the outcome of infection and disease progression. Current research interests in the department include understanding host signaling in response to viral infection, molecular mechanisms of NK and NK T cell activation, and molecular principles underlying fungal pathogenesis. This work provides an interdisciplinary structure for our training programs.
MMI supports undergraduate, graduate, and postdoctoral education in the areas of microbiology and immunology. Departmental instruction includes lecture courses, seminar courses, and laboratory research (both undergraduate independent study and graduate thesis). We foster collaborative studies within the department as well as with faculty in other departments, both on campus and hospital-based.
Congratulations to Jenna Wurster who has received an NSF Fellowship Award for her work in the Belenky Lab!
Congratulations to Benjamin Korry who has received an NSF Fellowship Award for his work in the Belenky Lab!
Microbial competition between Escherichia coli and Candida albicans reveals a soluble fungicidal factor
Localized and systemic fungal infections caused by Candida albicans can lead to significant mortality and morbidity. However, severe C. albicans infections are relatively rare, occurring mostly in the very young, the very old, and immunocompromised individuals. The fact that these infections are rare is interesting because as much as 80 percent of the population is asymptomatically colonized with C. albicans. It is thought that members of the human microbiota and the immune system work in concert to reduce C. albicans overgrowth through competition and modification of the growth environment. Here, we report that Escherichia coli (strain MG1655) outcompetes and kills C. albicans (strain SC5314) in vitro. We find that E. coli produces a soluble factor that kills C. albicans in a magnesium-dependent fashion such that depletion of available magnesium is essential for toxicity.
A central theme in biology is to understand how different signaling outputs can be accomplished by changes to signal transduction pathways. Here, we examined epigenetic differences between two cell states in the human fungal pathogen Candida albicans. We show that cells in the “white” state are sterile due to multiple bottlenecks in MAPK signaling relative to mating-competent “opaque” cells. Alleviation of these bottlenecks by reverse engineering effectively converts sterile white cells into sexually competent cells. These results have broad implications for understanding how epigenetic changes can impact MAPK expression and signaling output, including events associated with tumorigenesis. We also propose a model for how the white-opaque switch gained control of sexual reproduction in Candida during evolution.
Andrew G. Campbell, Dean of the Graduate School and a professor of medical science, has been quoted in Nature about the effect tax reforms will have on students in the sciences, especially historically under-represented groups.
Congratulations to Garvin Dodard on receiving the FASEB MARC Mentored Poster/Platform (Oral) Presententer Travel Award! The award assists with travel and registration fees for eligible underrepresented minority students and postdocs who are first time attendees at the AAI annual meeting. Garvin is one of seventeen recipients.
Andrew G. Campbell, Dean of the Graduate School and a professor of medical science, has been named a fellow of the American Society for Cell Biology (ASCB). One of the highest honors the society can bestow on its members, induction as a fellow recognizes Campbell’s sustained and significant impact on the discipline. The award, which went to 67 scientists and thought-leaders this year, acknowledges both long-term efforts to advance cell biology and its applications and service to the international community of cell biologists. The research program of Campbell’s lab focuses on Ribonuclease H.
Trypanosoma brucei employs multiple mechanisms to evade detection by its insect and mammalian hosts. The flagellar pocket (FP) is the exclusive site of uptake from the environment in trypanosomes and shields receptors from exposure to the host. The FP neck is tightly associated with the flagellum via a series of cytoskeletal structures that include the hook complex (HC) and the centrin arm. These structures are implicated in facilitating macromolecule entry into the FP and nucleating the flagellum attachment zone (FAZ), which adheres the flagellum to the cell surface.