The disordered C-terminal tail allows XRCC4-like factor (XLF) to find and bind the XRCC4-Lig4 complex, enabling DNA end synapsis and subsequent ligation during non-homologous end joining.

A combination of genetic and biochemical approaches suggest that yeast Rev7 promotes DNA double-strand break repair via NHEJ and inhibits homologous recombination by blocking Mre11 nuclease and Rad50’s ATPase activities.

Human papillomavirus type 8 E6 promotes alternative end joining by compromising non-homologous end joining and homologous recombination.

The human genome is unpackaged to allow DNA breaks to be joined back together, and then repackaged into chromosomes afterwards.

In concert phosphorylation site modification of both XRCC4 and XLF C-terminal disordered tails promotes disassembly of XRCC4/XLF DNA tethers during c-NHEJ.

Farrerol promotes the efficiency of CRISPR/Cas9-mediated genome editing in both cells and embryos.

Building on previous work (Jinek et al., 2013), we report a simple and robust system to achieve high fidelity and high efficiency (30% of homologous recombination) genome engineering by homology-directed repair pathway in human cells using cell cycle synchronization and timed delivery of Cas9 ribonucleoprotein complexes.

A viable separation of function XRCC4 knock-in mutant mouse model recapitulates some aspects of XRCC4 deficiency in humans, notably the absence of immune deficiency.

The 5' modification of the donor template facilitates highly efficient Crispr targeted homologous recombination and at the same time favors single copy integration.

Hundreds of proteins are involved in the DNA damage response but only three sensors for DSB were known but now SIRT6 is identified as a fourth DSB sensor.