Abstract
Dysfunctional telomeres arising either through natural attrition due to telomerase deficiency or by the removal of telomere binding proteins are recognized as double stranded breaks (DSBs). Repair of DSBs is crucial for the maintenance of genome stability. In mammals, DSBs are repaired by either error prone nonhomologous end joining (NHEJ) or error free homologous recombination (HR) and can be visualized as chromosomal fusions.