New insights into the DNA repair pathway choice with NuA4/TIP60

In eukaryotic cells, DNA double-strand breaks (DSBs) can be repaired through two main pathways, nonhomologous end-joining (NHEJ) or homologous recombination (HR). The selection of the repair pathway choice is governed by an antagonistic relationship between repair factors specific to each pathway, in a cell cycledependent manner. The molecular mechanisms of this decision implicate post-translational modifications of chromatin surrounding the break. Here, we discuss the recent advances regarding the function of the NuA4/ TIP60 histone acetyltransferase/chromatin remodeling complex during DSBs repair. In particular, we emphasise the contribution of NuA4/TIP60 in repair pathway choice, in collaboration with the SAGA acetyltransferase complex, and how they regulate chromatin dynamics, modify non-histone substrates to allow DNA end resection and recombination.

Automated summary

In eukaryotic cells, DNA double-strand breaks can be repaired through nonhomologous end-joining or homologous recombination. The choice of repair pathway is regulated by antagonistic relationship between repair factors specific to each pathway and is dependent on the cell cycle. The molecular mechanisms of this decision involve post-translational modifications of chromatin surrounding the break. Recent advances have focused on the function of the NuA4/TIP60 histone acetyltransferase/chromatin remodeling complex in DSBs repair, particularly its collaboration with the SAGA acetyltransferase complex and their role in regulating chromatin dynamics, DNA end resection, and recombination.