Michael Fasullo

Michael Fasullo

SUNY Polytechnic Institute
Associate Professor of Nanobioscience


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College of Nanoscale Sciences


  • Ph.D. (Biochemistry) Stanford University School of Medicine, Stanford, California
  • B.S. (Biology) 1979, Massachusetts Institute of Technology, Cambridge, Massachusetts

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

Description of 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. Dr. Fasullo’s research uses next generation sequencing for high- throuphput 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 Nanoscale Science and Engineering, University at Albany (SUNY at Albany) (2014-present)
  • Associate Professor, , College of Nanoscale Science and Engineering, State University of New York, Polytechnic Institute

Papers published

  1. Dong, Z. and Fasullo, M. Multiple recombination pathways for spontaneous and DNA damage-associated sister chromatid exchange in Saccharomyces cerevisiae: Role of RAD1 and the RAD52 epistasis group genes. Nucleic Acids Res. 31:2576-2585. 2003
  2. Fasullo, M, Zeng, L, and Gaillanza, P. Enhanced stimulation of chromosomal translocations by radiomimetic DNA damaging agents and camptothecin in Saccharomyces cerevisiae rad9 checkpoint mutants. Mutation Res. 547: 123-132, 2004
  3. Fasullo, M. and Dong, Z. Genetic control of sister chromatid recombination: the role of the radiation repair (RAD) genes. Current Genomics., 5:123-136, 2004
  4. Keller-Seitz, M., Certa, Ulrich, Sengstag, C., Wurgler, F., Sun, M., and Fasullo, M. Transcriptional response of the Yeast to the carcinogen aflatoxin B1: Recombinational repair involving RAD51 and RAD1. Molecular Biology of the Cell. 15:4321-4336, 2004
  5. DeMase, D., Zeng, L., Cera, C. and Fasullo, M. The Saccharomyces cerevisiae PDS1 and RAD9 checkpoint genes control different DNA double-strand break repair pathways. DNA Repair 4:59-69, 2005.
  6. Nag, D., Fasullo, M., Dong, Z., Tronnes, A. Inverted repeat-stimulated sister-chromatid exchange events are MSH2-dependent but RAD1 independent. Nucleic Acids Res. 33:5243-5249. 2005
  7. Fasullo, M. St. Amour, C., and Zeng, L., Enhanced stimulation of chromosomal translocations and sister chromatid exchanges by either HO-induced double-strand breaks or ionizing radiation in Saccharomyces cerevisiae yku70 mutants Mutation Res. 578:158-169, 2005
  8. Fasullo, M., Sun, M., Dong, Z., Saccharomyces cerevisiae RAD53 (CHK2) but not CHK1 is required for double-strand break-initiated SCE and DNA damage-associated SCE after exposure to X rays and chemical agents. DNA Repair 4: 1240-1251, 2005.
  9. 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
  10. 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
  11. 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
  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., Britton, A., Birch, A. Hypoxia enhances the replication of oncolytic herpes simplex virus in p53- breast cancer cells. Cell Cycle 8:1-4, 2009.
  14. 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.
  15. 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.
  16. 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.

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