The accurate replication of our DNA with minimal mutations or rearrangements is critical for human health. Microsatellites such as CAG repeats make up 3% of our genome and trinucleotide repeats within a genome can interfere with DNA replication and repair. Expanded CAG repeats can form secondary structures, for example hairpins, that can disrupt DNA replication and lead to fork stalling and collapse. Previous work in the Freudenreich Lab has shown that collapsed forks caused by expanded CAG repeats relocalize to the nuclear pore. Preliminary data has show that this process is dependent on sumoylation. I am interested in characterizing what proteins are required for relocalization of the collapsed fork to the nuclear pore and the role of protein sumoylation.