Michael Fasullo

Research Areas

• Genome profiling of toxin resistance
• Repair of radiation-induced DNA damage
• Cytochrome P450 activation of carcinogens
• Biosensors for toxin exposure
• Electrophoretic and single cell karyotyping

Research

Dr. Fasullo’s research focuses on understanding cellular responses to toxins and radiation. Human susceptibility to environmental and industrial toxins is highly variable. Genetic factors that contribute to toxin sensitivity are difficult to determine by epidemiological studies. Fasullo’s research uses next generation sequencing for high-throughput profiling of toxin resistance in model organisms to identify candidate human genes. He also uses budding yeast to characterize human cytochrome P450 polymorphisms that are associated with cancer susceptibility. He actively collaborates with researchers at University of California Berkeley and Northeastern University to develop new biosensors to rapidly characterize and identify chemical toxins. 

Professional Background

• Assistant Professor of Radiation Therapy, Loyola University School of Medicine, Loyola University of Chicago (1991-1996)
• Assistant Professor in Department of Molecular Biology and Biochemistry, The Albany Medical School (1996-2001)
• Associate Professor in the Center of Immunology and Microbial Disease, The Albany Medical School, (2001-2003)
• Senior Research Scientist, Ordway Research Institute (2003-2011)
• Associate Professor, Department of Biomedical Sciences, School of Public Health, University at Albany (2004-2013)
• Research Scientist, College of Nanotechnology, Science, and Engineering, University at Albany
• Associate Professor, College of Nanotechnology, Science, and Engineering, University at Albany

Papers published

1. Derevensky, M. and Fasullo, M. DNA damaging agents trigger the expression of the HML silent mating type locus in Saccharomyces cerevisiae. Mutat Res. 835:16-20. doi: 10.1016/j.mrgentox.2018.08.007. Epub 2018 Aug 24.
2. Fasullo, M., Thymidylate Depletion Stimulates Homologous Recombination by UNG1-dependent and UNG1-independent mechanisms in Saccharomyces cerevisiae. Annals of Mutagenesis 1:1005, 2017
3. De La Rosa, V. Y., Asfaha, J., Fasullo, M., Loguinov A.,  Li, P., Nakamura J., Swenberg, J.; Smith M. T., Vulpe, C.; Scelo D. G. Functional profiling in yeast reveals genotoxicity mechanisms and candidate susceptibility genes associated with trichloroethylene exposure and renal cell carcinoma. Toxicol Sci. 2017 Nov 1;160(1):111-120  Editor's Choice
4. Fasullo, M., Freedland, J., Cera, C., Egner P., Hartog, M., Ding, X.  An in vitro system for measuring genotoxicity mediated by human CYP3A4. Environ. Mol. Mutagen. 58:217-227, 2017.
5. Fasullo, M. and Sun, M. Both RAD5-dependent and independent pathways are involved in DNA damage-associated sister chromatid exchange in budding yeast.  AIMS Genetics, 4(2): 84-102, 2017 (special issue on DNA Repair).
6. Freedland, J., Cera, C., Fasullo, M. CYP1A1 I462V polymorphism is associated with reduced genotoxicity in yeast despite positive association with increased cancer risk. Mutation Research 815:35–43, 201
7. Fasullo, M. and Endres, L. Nucleotide Salvage Deficiencies, DNA Damage and Neurodegeneration. DNA Damage and Repair in Degenerative Diseases, International Journal of Molecular Sciences 16 (5), 9431-9449, 2015
8. Fasullo, M. Smith, A., Egner, P and Cera, C. Activation of Aflatoxin B1 by expression of CYP1A2 polymorphisms in Saccharomyces cerevisiae, Mutation Research 761:18-26, 2014.
9. Fasullo, M. Chen, Y., Bortcosh, W., Sun, M., Egner, P. Aflatoxin B1-associated DNA adducts stall S phase and stimulate Rad51 foci in S. cerevisiae. J Nucl. Acids. 2010.
10. Fasullo, M., Tsaponina, O., Sun, M., and Chabes, A., Elevated dNTP levels suppress hyper-recombination in Saccharomyces cerevisiae S-phase checkpoint mutants. Nucleic Acids Res. 38(4):1195-203, 2010.
11. Fasullo, M., Britton, A., Birch, A. Hypoxia enhances the replication of oncolytic herpes simplex virus in p53- breast cancer cells. Cell Cycle 8:1-4, 2009.
12. Fasullo, M. T. and Sun, M. UV but not X rays stimulate homologous recombination between sister chromatids and homologs in a Saccharomyces cerevisiae mec1 (ATR) hypomorphic mutant. Mutat. Res., 648: 73-81, 2008
13. Fasullo, M. T.  and Sun, M. The Saccharomyces cerevisiae checkpoint genes checkpoint genes RAD9, CHK1, and PDS1 are required for hyper-recombination in a Saccharomyces cerevisiae mec1 (ATR) hypomorphic mutant. Cell Cycle 7: 2418 – 2426, 2008
14. Fasullo, M.T., Sun, M., and Egner P. AFB1-DNA adducts stimulate both sister chromatid exchanges and mutation in Saccharomyces cerevisiae through a MEC1 (ATR), RAD53, DUN1-dependent pathway. Mol Carcinog. 47: 608-615, 2008
15. Sun, M. and Fasullo, M. T., Activation of the budding yeast securin Pds1 but not Rad53 correlates with double-strand break-associated G2/M cell cycle arrest in a mec1 hypomorphic mutant. Cell Cycle 6(15) 1896-1902, 2007