Associate Professor of Biology
B.A. - Carleton College
Ph.D. - University of Wisconsin-Madison
Phone - 540-568-5522 (113 Burruss)
Fax - 540-568-3333
Office - Bioscience 3016C
Courses: Genetics and Development (224)
Research Interests: Mechanisms of cell death in development and disease. Developmental processes of Caenorhabditis elegans.
My lab is interested in mechanisms of cell death, particularly those associated with apoptosis. During development and on into life, apoptosis eliminates unnecessary or badly damaged cells before they can adversely affect the health of the organism. Because the mechanisms that eliminate the cell are triggered within the cell itself, apoptosis is often referred to as “cellular suicide”. When apoptosis is inappropriately regulated, i.e. too active or not active enough, disease often results, ranging from neurodegenerative disorders to cancer. We study apoptosis in the model organism Caenorhabditis elegans, a small, genetically well-defined roundworm well-suited for this research. Using genetic, molecular biological and biochemical techniques, we are learning how apoptosis is repressed in healthy cells, and how that repression is released in cells fated to die. Because the core mechanism of apoptosis is highly similar between C. elegans and humans, we’re interested in using the results of our research to better understand how apoptosis is controlled in humans, and how that control is lost during the development of disease.
Arsenovic PT, Maldonado AT, Colleluori VD, Bloss TA. 2012. Depletion of the C. elegans NAC engages the unfolded protein response, resulting in increased chaperone expression and apoptosis. PLoS One. 7(9):e44038.
Bloss, T. A., E. S. Witze, and J. Rothman. 2003. Suppression of CED-3-independent apoptosis by mitochondrial betaNAC in Caenorhabditis elegans. Nature 424: 1066-1071.
Bloss, T., A. Kaykas, and B. Sugden. 1999. Dissociation of patching by latent membrane protein-1 of Epstein-Barr virus from its stimulation of NF-kappaB activity. J. Gen Virol. 80: 3227-3232.