David M. Wilson, Ph.D.

Senior Investigator

Laboratory of Molecular Gerontology

NIA

251 Bayview Boulevard
Suite 100
Baltimore, MD 21224

410-558-8153

wilsonda@mail.nih.gov

Research Topics

Base Excision Repair: Base excision repair (BER) is the major pathway for correcting most spontaneous and oxidative DNA damage. In brief, the main steps of BER consist of: (1) excision of the damaged base (e.g. 8-oxoguanine), (2) incision of the DNA backbone at the abasic site product, (3) removal of the abasic terminal fragment, (4) gap-filling synthesis, and (5) ligation of the final nick. Our focus has been to understand the molecular mechanisms of repair of abasic sites and oxidative DNA single strand breaks, and to define the coordinated effort between the proteins of BER. Towards this end, we have isolated several BER proteins and have developed biochemical assays to assess their individual and cooperative structure-function relationships.

Biography

Dr. David Wilson completed his Ph.D. work in 1993 at Loyola University of Chicago, Stritch School of Medicine, as part of the Molecular Biology Program. Dr. Wilson then performed his postdoctoral research training at the Harvard School of Public Health until 1997, when he became a Senior Biomedical Scientist at Lawrence Livermore National Laboratory in the Biology and Biotechnology Research Program. While at Livermore, he was also briefly an adjunct faculty member at the University of California, Davis. Dr. Wilson started his present position at NIA in 2002.

Selected Publications

  1. Illuzzi JL, McNeill DR, Bastian P, Brenerman B, Wersto R, Russell HR, Bunz F, McKinnon PJ, Becker KG, Wilson DM 3rd. Tumor-associated APE1 variant exhibits reduced complementation efficiency but does not promote cancer cell phenotypes. Environ Mol Mutagen. 2017;58(2):84-98.

  2. Iyama T, Lee SY, Berquist BR, Gileadi O, Bohr VA, Seidman MM, McHugh PJ, Wilson DM 3rd. CSB interacts with SNM1A and promotes DNA interstrand crosslink processing. Nucleic Acids Res. 2015;43(1):247-58.

  3. Scheibye-Knudsen M, Tseng A, Borch Jensen M, Scheibye-Alsing K, Fang EF, Iyama T, Bharti SK, Marosi K, Froetscher L, Kassahun H, Eckley DM, Maul RW, Bastian P, De S, Ghosh S, Nilsen H, Goldberg IG, Mattson MP, Wilson DM 3rd, Brosh RM Jr, Gorospe M, Bohr VA. Cockayne syndrome group A and B proteins converge on transcription-linked resolution of non-B DNA. Proc Natl Acad Sci U S A. 2016;113(44):12502-12507.

  4. Iyama T, Wilson DM 3rd. Elements That Regulate the DNA Damage Response of Proteins Defective in Cockayne Syndrome. J Mol Biol. 2016;428(1):62-78.

  5. Sykora P, Kanno S, Akbari M, Kulikowicz T, Baptiste BA, Leandro GS, Lu H, Tian J, May A, Becker KA, Croteau DL, Wilson DM 3rd, Sobol RW, Yasui A, Bohr VA. DNA polymerase beta participates in mitochondrial DNA repair. Mol Cell Biol. 2017.


This page was last updated on August 11th, 2017