Homologous recombination (HR) is the process used by DNA sequences to recover missing genetic information at the site of a double stand break (DSB). An essential aspect of HR that remains poorly understood is the mechanism of homology search. To study this aspect of HR in diploid yeast cells, a fluorescent chromosome tagging system was used to track chromosome mobility of the two homologs in response to DSBs. We previously found that yeast cells dramatically increase their chromosome mobility in response to DSBs. This response has two components: the first is a large “local” increase in the mobility of the cut chromosome; the second is a smaller “global” increase in mobility at other undamaged sites in the genome (including the homolog). The MRX complex, consisting of Mre11, Rad50, and Xrs2 proteins, plays multiple roles in HR; such as processing broken DNA ends and initiating DNA damage checkpoint signaling. Because of its multiple roles, we hypothesized that MRX would play a role in regulating chromosome mobility. To test this hypothesis we deleted Mre11, the protein-scaffolding component of the complex in cells with our chromosome tagging system. Chromosome mobility was assayed both before and after DNA damage. We find that when a site-specific DSB is induced with I-SceI at the tagged locus in an mre11∆ strain, the local mobility of that site is greatly delayed. However, when the same mutant cells are treated with 40 Gy of ionizing radiation (IR), producing ~ 4 random DSBs in the genome, mobility of the tagged locus displays a normal global mobility response. This global mobility response can be blocked by inhibition of the PI3K checkpoint kinases using caffeine. In addition, we find that IR treatment of mre11Δ cells results in an increase in the number of both Rad51 and Rad52 foci that is indistinguishable from wild type cells. In contrast, accumulation of Rad51 and Rad52 foci after a site-specific DSB is delayed compared to a wild type strain. We propose that a single DSB requires resection initiation by the MRX complex to generate checkpoint dependent mobility, whereas, IR treatment rapidly results in checkpoint dependent DNA mobility due to the accumulation of multiple processed ends created by alternative means. Finally, we observe that pairing between tagged homologous chromosomes after induction of a site specific DSB is a delayed in a mre11Δ strain. This delay correlates with the observed delay in local mobility, supporting a model in which local mobility is necessary for pairing of homologous chromosomes.