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

DNA Damage and L1 Retrotransposition

1Department of Pathology and Laboratory Medicine, School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
2405B Stellar Chance Labs, University of Pennsylvania, 422 Curie Boulevard, Philadelphia, PA 19104, USA

Received 22 August 2005; Accepted 16 October 2005

Copyright © 2006 Evan A. Farkash and Eline T. Luning Prak. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.