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 three 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 have now developed a knock-in mouse model to further explore the physiological relevance of E2F1 in the DNA damage response.

The second 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.

The third area of research is the development of mouse models for the human p53 R72P polymorphism. This single nucleotide polymorphism (SNP) has been linked to increased risk for a variety of cancers. In vitro studies also indicate that the two p53 variants have different biochemical and biological properties, particularly in their apoptotic properties. These mouse models are being used to understand the molecular mechanism by which this p53 polymorphism modulates the response to carcinogenic agents and the development of cancer

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. Paulson QX, Pusapati RV, Hong S, Weaks RL, Conti CJ, Johnson DG. Transgenic expression of E2F3a causes DNA damage leading to ATM-dependent apoptosis, Oncogene, 27 (36), 4954-61, 2008
  3. 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
  4. Russell JL, Weaks RL, Berton TR, Johnson DG. E2F1 suppresses skin carcinogenesis via the ARF-p53 pathway, Oncogene, 25 (6), 867-76, 2006
  5. 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

Contact Information


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