DNA double strand break repair

DNA Double Strand breaks are the most citotoxic DNA lesions. When left completely unrepaired they cause cellular and embryonic lethality. However, mutations that affect but not block their repair cause an increase in genomic instability, a driving force in cancer development and the molecular root of several rare genetic diseases. The phenotypes associated to defective DNA double starnd break repair vary enormously. DNA double strand breaks are repaired basically by two alternative pathways that compete for the same substrate. The ends of the break can be simply ligates with little or no processing in a mechanisms known as non-homologous end-joining (NHEJ). On the other hand, the DNA ends can be processed in order to be repaired by a more complex mechanism called homologous recombination. The correct use of either of them is key to maintain genomic stability and, therefore, for human health.