Mitchell, David L.

Mitchell, David L. Ph.D.

Selected Publications  |  Search PubMed  |  Contact

Research Interests

UV photochemistry, photobiology and photocarcinogenesis, DNA repair, UV environmental photobiology

Current Research

The overall objective of our research is to understand the molecular and biological responses of cells to DNA damage resulting from solar ultraviolet (UV) radiation. From these studies we hope to better understand the molecular basis of sunlight-induced skin cancer in man. Several aspects of this problem are currently under study.

  • We have shown that DNA damage caused by sunlight accumulates in a subset of basal epidermal cells and that these cells may be responsible for initiating the events that lead to skin cancer. Research efforts are underway to determine if these cells are stem cells, what mechanisms are involved in damage accumulation in these cells (i.e., DNA repair), what triggers these cells to divide, and whether or not these cells are precursors of skin cancer.
  • We are involved in a group effort to explore the genetics and mechanisms underlying melanoma using a Xiphophorus (platyfish/swordtail) fish hybrid system. To date our studies have focused on describing phenotypic variation in DNA repair with particular attention to how these phenotypes are inherited and the consequences for melanoma susceptibility. Of particular interest has been the question of how DNA damage is involved in melanoma; specifically whether the direct damage to DNA caused by UVB light or indirect free radical damage caused by UVA light is important. We currently have a large study underway to examine the efficacy of UVA and UVB radiation on melanoma formation in a specific UV-susceptible backcross hybrid. In addition we are cloning genes that may impact melanoma susceptibility or resistance and will be looking at the expression of these genes and polymorphisms in tumor-bearing and non-bearing fish.
  • We have shown that expression of the E2F1 gene in mice correlates with the efficiency of nucleotide excision repair. We are currently studying the mechanism by which E2F1 (and other transcription factors) influence the nucleotide excision repair process, particularly at the very early detection phase of repair, and the role of E2F1 in accessibility of the DNA damage in chromatin.
  • From our interest in the effects of stratospheric deozonation on the environment and human health, we have engaged in studies on how geographical and latitudinal differences in UVB affect marine plankton populations, with particular focus on bacterioplankton UV responses and adaptations. In addition, we have been involved in a large multi-investigator study of the effects of season and temperature on the UV response across a broad trophic spectrum of planktonic organisms in fresh water lakes.

Selected Publications

  1. Mitchell D, Willerslev E, Hansen A. Damage and repair of ancient DNA, Mutat Res F, 571 (1-2), 265-76, 2005
  2. Berton TR, Mitchell DL, Guo R, Johnson DG. Regulation of epidermal apoptosis and DNA repair by E2F1 in response to ultraviolet B radiation, Oncogene, 24 (15), 2449-60, 2005
  3. Willerslev E, Hansen AJ, Ronn R, Brand TB, Barnes I, Wiuf C, Gilichinsky D, Mitchell D, Cooper A. Long-term persistence of bacterial DNA, Curr Biol, 14 (1), R9-10, 2004
  4. Mitchell DL, Nairn RS, Johnston DA, Byrom M, Kazianis S, Walter RB. Decreased levels of (6-4) photoproduct excision repair in hybrid fish of the genus Xiphophorus, Photochem Photobiol, 79 (5), 447-52, 2004
  5. MacFayden EJ, Williamson CE, Grad G, Lowery M, Jeffrey WH, Mitchell DL. Molecular response to climate change: temperature dependence of UV-induced DNA damage and repair in the freshwater crustacean Daphnia pulicaria, Global Change Biol, 10 (4), 408-16, 2004

Contact Information


Mailing Address: P.O. Box 389, Smithville, Texas 78957
Physical Address: 1808 Park Road 1C, Smithville, Texas 78957
Phone: (512) 237-9424