Mutagenesis plays a central role in our lives. A low level of mutagenesis is advantageous, and ensures the survival of species by promoting evolution. Programmed mutagenesis of immunoglobulin genes promotes diversity and provides a dynamic defense against invading pathogens. However, many human diseases, including most cancers, arise as a consequence of mutations that occur either spontaneously, or are induced by environmental chemical/physical mutagens. Accumulation of oxidative lesions as a result of normal metabolism has been implicated in premature aging and neurodegeneration. Mutagenesis also drives the evolution of virulent bacterial and viral pathogens, allowing them to evolve resistance to therapeutics and thwart the immune response.

The 2008 Mutagenesis Gordon Conference will focus on the molecular mechanisms of mutagenesis that gives rise to genomic instability. In particular, the meeting will enhance our understanding of how mutagenesis occurs in the course of DNA replication and the immune response, and how mutagenesis leads to human genetic disease, cancer, neurodegeneration, and promotes aging. Over the course of four days, morning and evening sessions will focus on: (i) Mutagenesis due to blocked replication and transcription; (ii) Consequences of oxidative stress; (iii) Recombination induced genomic instability; (iv) Physiological mutagenesis in the immune response; (v) Rare human diseases associated with genomic instability, neurodegeneration and premature aging; (vi) Low-fidelity replication and cancer; (vii), Mechanisms of mutagenesis; and (viii) Signaling for repair; a mechanism to avoid excessive mutagenesis.

It is anticipated that the conference will attract a maximum of 150 scientists with diverse interests and experimental approaches and that the informal setting at Magdalen College will foster discussions and the establishment of collaborations that lead to novel scientific discoveries.