In mammalian cells, DNA double-strand breaks (DSBs) are repaired by the non-homologous end-joining (NHEJ) pathway. A key component of this repair mechanism is the DNA binding protein, Ku. A recent study shows that Par-3, a protein involved in cell polarity and the assembly of tight junctions, interacts with Ku and is involved in NHEJ, suggesting an intriguing new role for Par-3 and links between cell morphology and DNA damage response pathways.
