Johnson, David G.

Johnson, David G. Ph.D.

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Research Interests

Cancer genetics; DNA damage response; apoptosis; cell cycle

Current Research

My current research is focused on two main areas. The first involves the role of the E2F1 transcription factor in the response to DNA damage. In particular, we are interested in exploring a direct, non-transcriptional role for E2F1 in the repair of several types of DNA damage, including double-strand breaks and UV-induced photoproducts. We find that phosphorylation of E2F1 by ATM or ATR at serine 31 leads to the accumulation of E2F1 at sites of DNA damage. Our studies indicate that E2F1 stimulates efficient repair by recruiting the GCN5 histone acetyltransferase and other chromatin modifying enzmes to sites of damage to facilitate access to the DNA repair machinery. We are now developing a knock-in mouse model to further explore the physiological relevance of E2F1 in the DNA damage response.

The other area of research is examining how the deregulated expression of oncogenes is sensed by the cell and the role of the oncogenic stress response in suppressing tumorigenesis. We have found that overexpression of the oncogenic transcription factors Myc and E2F3 causes DNA breaks, both in vitro and in vivo, and we are trying to understand how this damage arises. We have also found that the ATM kinase is involved in sensing oncogene-induced DNA damage and is important for activating p53 and inducing apoptosis in response to oncogenic stress. We are now examining the role of other components of the ATM network in sensing oncogene-induced DNA damage and suppressing the development of cancer.

In addition to these two main areas of research, we are also developing and characterizing humanized mouse models for the p53 R72P polymorphism. These models will be used to explore the role of this human single nucleotide polymorphism (SNP) in modulating cancer susceptibility and the response to therapy.

Selected Publications

  1. Hong S, Paulson QX, Johnson DG. E2F1 and E2F3 activate ATM through distinct mechanisms to promote E1A-induced apoptosis, Cell Cycle, 7 (3), 391-400, 2008
  2. Pusapati RV, Rounbehler RJ, Hong S, Powers JT, Yan M, Kiguchi K, McArthur MJ, Wong PK, Johnson DG. ATM promotes apoptosis and suppresses tumorigenesis in response to Myc, Proc Natl Acad Sci U S A, 103 (5), 1446-51, 2006
  3. Russell JL, Weaks RL, Berton TR, Johnson DG. E2F1 suppresses skin carcinogenesis via the ARF-p53 pathway, Oncogene, 25 (6), 867-76, 2006
  4. 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
  5. Powers JT, Hong S, Mayhew CN, Rogers PM, Knudsen ES, Johnson DG. E2F1 uses the ATM signaling pathway to induce p53 and Chk2 phosphorylation and apoptosis, Mol Cancer Res, 2 (4), 203-14, 2004
  6. Rounbehler RJ, Rogers PM, Conti CJ, Johnson DG. Inactivation of e2f1 enhances tumorigenesis in a myc transgenic model, Cancer Res, 62 (11), 3276-81, 2002
  7. Russell JL, Powers JT, Rounbehler RJ, Rogers PM, Conti CJ, Johnson DG. ARF differentially modulates apoptosis induced by E2F1 and Myc, Mol Cell Biol, 22 (5), 1360-8, 2002

Contact Information


Mailing Address: P.O. Box 389, Smithville, Texas 78957
Physical Address: 1808 Park Road 1C, Smithville, Texas 78957
Phone: (512) 237-9438