Reviews

< Previous         Next >  
Prevention of DNA re-replication in eukaryotic cells Free
Lan N. Truong and Xiaohua Wu*
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA *Correspondence to:Xiaohua Wu, E-mail: xiaohwu@scripps.edu
J Mol Cell Biol, Volume 3, Issue 1, February 2011, 13-22,  https://doi.org/10.1093/jmcb/mjq052
Keyword: DNA re-replication, cell cycle checkpoints, DNA damage response, Cdt1, DSB repair, genome stability, tumorigenesis
DNA replication is a highly regulated process involving a number of licensing and replication factors that function in a carefully orchestrated manner to faithfully replicate DNA during every cell cycle. Loss of proper licensing control leads to deregulated DNA replication including DNA re-replication, which can cause genome instability and tumorigenesis. Eukaryotic organisms have established several conserved mechanisms to prevent DNA re-replication and to counteract its potentially harmful effects. These mechanisms include tightly controlled regulation of licensing factors and activation of cell cycle and DNA damage checkpoints. Deregulated licensing control and its associated compromised checkpoints have both been observed in tumor cells, indicating that proper functioning of these pathways is essential for maintaining genome stability. In this review, we discuss the regulatory mechanisms of licensing control, the deleterious consequences when both licensing and checkpoints are compromised, and present possible mechanisms to prevent re-replication in order to maintain genome stability.