Journal of Biomedicine and Biotechnology 
Volume 2006 (2006), Article ID 37285, 8 pages
doi:10.1155/JBB/2006/37285
Review Article

DNA Damage and L1 Retrotransposition

Evan A. Farkash1 and Eline T. Luning Prak1,2

 1Department of Pathology and Laboratory Medicine, School of Medicine, University of Pennsylvania, Philadelphia 19104, PA, USA
2405B Stellar Chance Labs, University of Pennsylvania, 422 Curie Boulevard, Philadelphia 19104, PA, USA
Received 22 August 2005; Accepted 16 October 2005

Abstract

Barbara McClintock was the first to suggest that transposons are a source of genome instability and that genotoxic stress assisted in their mobilization. The generation of double-stranded DNA breaks (DSBs) is a severe form of genotoxic stress that threatens the integrity of the genome, activates cell cycle checkpoints, and, in some cases, causes cell death. Applying McClintock's stress hypothesis to humans, are L1 retrotransposons, the most active autonomous mobile elements in the modern day human genome, mobilized by DSBs? Here, evidence that transposable elements, particularly retrotransposons, are mobilized by genotoxic stress is reviewed. In the setting of DSB formation, L1 mobility may be affected by changes in the substrate for L1 integration, the DNA repair machinery, or the L1 element itself. The review concludes with a discussion of the potential consequences of L1 mobilization in the setting of genotoxic stress.