Academic Education:

B.Sc. Biology. Pontificia Universidad Catolica de Valparaiso. Valparaiso-Chile
Licensure in Science. Biology. Pontificia Universidad Catolica de Valparaiso. Valparaiso-Chile
Ph.D. Molecular Biology and Microbiology. Tufts University Medical School. Boston.

Appointments:

Department of Biology, M.I.T. Postdoctoral Associate. (1995-1999)

Department of Biology, M.I.T. Research Scientist. (1999-2005)

Department of Biology. Northeastern University. (2005-present)

Other Professional Activities:

Graduate Coordinator, Department of Biology, Northeastern University (1995-1999)

Director, Behavioral Neuroscience Major, Northeastern University (1999-2001, 2009-)

Advisory Board Journal of Biological Rhythms (1994-1995)

Executive Committee, Society for Research on Biological Rhythms (1998-2000)

Treasurer, Society for Research on Biological Rhythms (2002-2004)

Regular Member, NIH Center for Scientific Review, Biological Rhythms and Sleep Study Section (2000-2004)

Research Interests:

At the molecular level, networks are given by multiple interactions of nucleic acids and proteins and by protein-protein interactions. The latter results, for the most part, in formation of multiple protein complexes (MPCs).

My research group is interested in studying an MPC formed by components involved in important DNA transactions when cells are exposed to DNA damage. This is a condition that induces the expression of error-prone DNA polymerases, the activity of which might lead to mutations. Our long-term goal is to learn about the mechanisms that regulate the activity of error-prone Y family DNA polymerases. This will provide a detailed understanding of the mutation pathways effected by Y DNA polymerases in bacteria. In turn, this will lead to a good understanding of the involvement of error prone Y family DNA polymerases in the evolution of important functions such as antibiotic resistance. Importantly, our research will contribute to the general understanding of mutagenesis, since Y family polymerases are conserved from bacteria to humans

Our working model is that protein-protein interactions, and likely MPC formation, modulate the activity of Y family DNA polymerases allowing to sculpt mutagenesis that might permit survival in conditions of stress.

We use bacteria as a model system and especially Escherichia coli. Due to its relative simplicity, studying basic processes in bacteria will render mechanistic insights that would be difficult to attain directly in more complex systems.

Teaching Activities:

I have taught at the Pontificia Universidad Catolica de Valparaiso (Chile), Tufts Medical School, MIT, and Northeastern University. These teaching activities include laboratory classes and lectures courses in molecular biology, bacterial genetics, biochemistry, and microbiology.

Selected Publications:

Godoy V. G.*, Jarosz D. F.*, Simon S. M., Abyzov, A., Ilyin, V., and G. C. Walker. 2007. UmuD and RecA directly modulate the mutagenic potential of the Y family DNA polymerase DinB. Molecular Cell. vol 28 (December 28):1058-1070

Godoy V.G., Jarosz D.F., Walker F., Simmons L., and G. C. Walker. 2006. Y Family DNA polymerases respond to DNA damage-independent inhibition of replication fork progression. EMBO J. vol 25(4):868-79

Jarosz D.F.*, Godoy V.G.*, Delaney J.C., Essigman J.M., and G. C. Walker. 2006. A single aminoacid governs enhanced activity of DinB DNA polymerase on damaged templates. Nature. vol 439 (7073): 225-228

Godoy V.G., F.S. Gizatullin and M. S. Fox. 2000. Some features of the mutability of bacteria during non-lethal selection. Genetics., vol. 154: p.49-59. Genetics Society of America

Godoy V.G., M.M. Dallas, T.A. Russo and M.H. Malamy. 1993. A role for Bacteroides fragilis neuraminidase in bacterial growth in two model systems. Infection and Immunity, vol.61: p. 4415-4426. American Society for Microbiology.

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