The linear ends of natural chromosomes (telomeres) should resemble internal genome scissions. For the stability of cells it is imperative that telomeres avoid eliciting a DNA damage response. Yet recent data has shown that DNA damage repair proteins involved in homologous recombination repair are localized to the telomeres during the cell cycle. In this dissertation, I have further examined the role of HR proteins at the telomeres in the model organism C. elegans, and have found that HR proteins are required for the proper processing and maintenance of telomeres. Further, by examining the extra-chromosomal t- circles in C. elegans strains with HR proteins disrupted, I have shown that HR protein disruption leads to a decrease in t-circles. These data strongly suggest that t- circles are a byproduct of t-loop formation