2004 Mutagenesis Gordon Conference

Gordon Research Conferences, East Greenwich RI

Investigators

Abstract

DESCRIPTION (provided by applicant): Funds are requested to support travel and/or conference fees for scientists attending the 14th bi-annual Gordon Research Conference on Mutagenesis to be held at The Queen's College, Oxford, UK, September 12-17, 2004. The Conference will focus on the basic mechanisms of mutagenesis and DNA repair, and also will emphasize the biological implications of mutations in terms of evolutionary processes and human disease. Selected speakers will be experts in the field of mutagenesis, and the meeting will serve as a forum for extensive interactions among all attending scientists through open discussions within each session as well as poster presentations. The Conference is usually heavily oversubscribed, with attendance being limited to 135 participants. Specific efforts will be made and special consideration given to encouraging the attendance of minority groups, women, graduate students, and persons with disabilities. The conference will open on the first evening with two keynote addresses that will provide a historical perspective on the field of mutagenesis. This will be followed by eight formal morning/evening sessions focusing on: (i) mutagenic systems, (ii) hypermutable sequences, (iii) mechanisms of mutation, (iv) mutation avoidance systems, (v) mutation in human hereditary and infectious diseases, (vi) mutation rates in evolution and genotypephenotype relationships, (vii) ecology, mutagenesis and the modeling of evolution and (viii) genetic diversity of the human population and models for human mutagenesis. The Conference will close with a keynote lecture that will provide a synthesis of the results and ideas presented at the meeting. The field of mutagenesis is critical to human health because mutations initiate and facilitate the progression of a multitude of human diseases, especially cancer and neurodegenerative diseases. In addition, mutagenic processes are important in controlling host-parasite interactions, and the accumulation of oxidative damage has been implicated in aging.