Impact of Transposable Elements on DNA Double-Strand Break Repair and Genomic Stability

Transposable elements (TEs) are indispensable components of eukaryotic genomes, mechanistically linked to carcinogenesis, aging and other degenerative diseases. The ability of TEs to self-propagate and cause deletions, inversions or insertions within the genome poses a real threat to the fidelity of genomic integrity. This review discusses the fundamental properties of TEs, with a focus on cellular interactions associated with mechanisms involved in recombination, replication, and DNA repair. Since mobilization of TEs induces double-strand breaks (DSBs), faulty repair mechanisms could lead to cellular dysfunction, pathology and death. The TE-induced DNA DSB repair cascade follows either homologous recombination (HR) or non-homologous end-joining (NHEJ) pathways. Importantly, epigenetic regulatory mechanisms including DNA methylation and histone acetylation provide additional control in ensuring accurate DNA repair and could prove to be key targets for therapeutic intervention.