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A Third Link connecting Aging with Double Strand Break Repair
William R. Engels, Dena M. Johnson-Schlitz, Carlos Flores, Lisa White and Christine Preston
volume 6 | issue 2
15 January 2007Pages: 131 - 135
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Until recently, the connection between aging and DNA repair has rested on two classes of observation. First, DNA damage and unrepaired double-strand breaks (DSBs) accumulate with age. Second, several defects in DNA repair genes are associated with early onset of age-related diseases and other signs of premature aging. Now, a third link has emerged: The mechanisms by which cells repair DSB damage can change dramatically with age, shifting from simpler end-joining processes in younger organisms to homologous mechanisms in which missing genetic information is restored through use of a template. So far this third link between aging and DNA repair has only been observed in a small number of experimental systems, and cannot yet claim the generality of the other two. Here we review the evidence for this phenomenon and present new data testing models for the underlying causes. If the generality of age-related changes in DSB repair pathway usage can be established, it will provide a new insight into the underlying molecular basis of aging and how evolution has shaped these processes.
Authors
William R. Engels
Univeristy of Wisconsin; Madison, Wisconsin USA
Dena M. Johnson-Schlitz
Univeristy of Wisconsin; Madison, Wisconsin USA
Carlos Flores
Univeristy of Wisconsin; Madison, Wisconsin USA
Lisa White
Univeristy of Wisconsin; Madison, Wisconsin USA
Christine Preston
Univeristy of Wisconsin; Madison, Wisconsin USA
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.




