Graduate Studies Faculty
Michael Forte, Ph.D.
Programs:Cell & Developmental Biology
Molecular & Medical Genetics
Neuroscience Graduate Program
Program in Molecular & Cellular Biosciences
Research Interests:mitochondria, neurodegeneration, axonal targeting, Neurobiology of Disease » Click here for more about Dr. Forte's research » PubMed Listing
Preceptor RotationsDr. Forte has not indicated availability for preceptor rotations at this time.
Faculty MentorshipDr. Forte has not indicated availability as a mentor at this time.
Michael Forte is a senior scientist at the Vollum Institute and a professor in the Departments of Molecular and Medical Genetics, Cell and Developmental Biology, and Physiology and Pharmacology in the School of Medicine. After being awarded his B.S. from the University of Notre Dame in 1973, Forte earned his Ph.D. in Genetics from the University of Washington in 1978. He then went to the University of Wisconsin for four years of postdoctoral research in Molecular Biology. In 1982, Forte became an assistant professor at Case Western Reserve University, where he remained until his appointment to the Vollum in 1986.
Summary of Current Research
The Forte lab is investigating the role of mitochondria in the overall regulation of cellular calcium (Ca2+). Ca2+ ions probably represent the most ubiquitous signaling pathway in all cells. Mitochondria are now recognized as initiators and transducers of a range of cell signals, participating in neuronal functions like synaptic plasticity and processes central to activation and amplification of programmed cell death. Moreover, as the main source of cellular ATP, mitochondria must respond to fluctuating energy demands of the cell. As local and global fluctuations in Ca2+ concentration are ubiquitous in eukaryotic cells and are the common factor in a wide array of intra- and inter-cellular signaling cascades, the relationships between mitochondrial function and Ca2+ transients is currently a subject of intense scrutiny. The mitochondrial Ca2+ pool oscillates rapidly in synchrony with cytosolic Ca2+ and thus, mitochondria have the ability to shape cytosolic Ca2+ transients. Mitochondria also respond to Ca2+ uptake by upregulating energy production, thus integrating metabolism with local Ca2+ signaling. The Forte lab is interested in the reciprocal effects of Ca2+ on mitochondria and mitochondria on the Ca2+ signals. Using genetic approaches in mice and Drosophila, the goal is to understand the response of mitochondria to Ca2+, the pathways by which Ca2+ accumulates into mitochondria, and the potential role of mitochondrial Ca2+ in neurodegenerative disease processes. Our studies focus on two pathways by which mitochondrial Ca2+ levels are modulated.
Su KG, Savino C, Marracci G, Chaudhary P, Yu X, Morris B, Galipeau D, Giorgio M, Bourdette D*, and Forte M*. (2012) Genetic inactivation of p66ShcA is neuroprotective in a model of multiple sclerosis. Eur. J. Neurosci. 35:562-571. *co-senior authors
Barsukova AG, Forte M*, and Bourdette B*. (2012) Focal increases of axoplasmic Ca2+, aggregation of sodium-calcium exchanger, N-type Ca2+ channel, and actin define the sites of spheriods axons undergoing oxidative stress. J. Neurosci. 32:12028-12037. *co-senior authors
Barsukova A, Komarov A, Hajnóczky G, Bernardi P, Bourdette D, and Forte M. (2011) Activation of the mitochondrial permeability transition pore modulates Ca2+ responses to physiological stimuli in adult neurons. Eur. J. Neurosci. 33:831-842.
Su KG, Banker G, Bourdette D, and Forte M. (2009) Axonal degeneration in multiple sclerosis: the mitochondrial hypothesis. Curr. Neurol. Neurosci. Rep. 9:411-417.
Basso E, Petronilli V, Forte M*, and Bernardi P.* (2008) Phosphate is essential for inhibition of the mitochondrial permeability transition pore by cyclosporin A and by cyclophilin D ablation. J. Biol. Chem. 283:26307-26311. *co-senior authors.
Forte M, Gold BG, Marracci G, Chandhary P, Basso E, Johnsen D, Yu X, Fowlkes J, Rahder M, Stem K, Bernardi P, and Bourdette D. (2007) Cyclophilin D inactivation protects axons in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Proc. Nat. Acad. Sci. USA 104:7558-7563.