Dragony Fu


Contact Information

Dragony Fu
Assistant Professor
Office: Hutchison 333
Office Hours: By appointment
Phone: (585) 276-3346
Lab Website
Research Interests: DNA repair mechanisms; Genotoxic stress response pathways; Programmed cell death  

Research Overview

Our laboratory investigates the cellular stress response pathways that determine cell fate after exposure to cytotoxic and mutagenic damaging agents. To study the diverse processes involved in the stress response, we use an integrated approach combining biochemistry, molecular biology and cell physiology in mammalian tissue culture systems and genetic mouse models. Through this approach, we have discovered novel targets and functions for proteins involved in DNA repair, RNA modification and programmed cell death. Since DNA damage poses a significant threat to genome integrity and cellular viability, a greater understanding of the molecular mechanisms that respond to DNA damage will provide critical insight into multiple aspects of human health, including cancer prevention and therapy, degenerative disorders and aging.

Our research encompasses:

  • Nucleic acid repair and modification
  • Regulation of protein translation in response to genotoxic stress
  • Programmed necrotic cell death induced by DNA damage


Selected Publications

  • Fu, D., Jordan, J. J. and Samson, L. D. (2013). "Human ALKBH7 is required for alkylation and oxidation-induced programmed necrosis." Genes & Development 27(10): 1089-1100.
  • Fu, D., Calvo, J. A. and Samson, L. D. (2012). "Balancing repair and tolerance of DNA damage caused by alkylating agents."Nature Reviews Cancer 12(2): 104-120.
  • Fu, D. and Samson, L. D. (2011). "Direct repair of 3,N(4)-ethenocytosine by the human ALKBH2 dioxygenase is blocked by the AAG/MPG glycosylase." DNA Repair.
  • Fu, D., Brophy, J. A., Chan, C. T., Atmore, K. A., Begley, U., Paules, R. S., Dedon, P. C., Begley, T. J. and Samson, L. D. (2010). "Human AlkB homolog ABH8 Is a tRNA methyltransferase required for wobble uridine modification and DNA damage survival." Molecular and Cellular Biology 30(10): 2449-2459.
  • Errington, T. M., Fu, D., Wong, J. M. and Collins, K. (2008). "Disease-associated human telomerase RNA variants show loss of function for telomere synthesis without dominant-negative interference." Molecular and Cellular Biology 28(20): 6510-6520.
  • Fu, D. and Collins, K. (2007). "Purification of human telomerase complexes identifies factors involved in telomerase biogenesis and telomere length regulation." Molecular Cell 28(5): 773-785.
  • Fu, D. and Collins, K. (2006). "Human telomerase and Cajal body ribonucleoproteins share a unique specificity of Sm protein association." Genes & Development 20(5): 531-536.
  • Fu, D. and Collins, K. (2003). "Distinct biogenesis pathways for human telomerase RNA and H/ACA small nucleolar RNAs."Molecular Cell 11(5): 1361-1372.