DNA non-homologous end-joining enters the resection arena

DNA non-homologous end-joining enters the resection arena

[Non-homologous DNA end joining].

DNA double strand breaks (DSB) are the most serious form of DNA damage. Repair of DSBs is important to prevent chromosomal fragmentation, translocations and deletions. Non-homologous end joining (NHEJ) is one of three major pathways for the repair of DSBs in human cells. In this process two DNA ends are joined directly, usually with no sequence homology, although in the case of same polarity of...

Modeling non-homologous end joining.

Non-homologous end joining (NHEJ) is an important DNA repair pathway for DNA double-strand breaks. Several proteins, including Ku, DNA-PKcs, Artemis, XRCC4/Ligase IV and XLF, are involved in the NHEJ for the DNA damage detection, DNA free end processing and ligation. The classical model of NHEJ is a sequential model in which DNA-PKcs is first recruited by the Ku bound DNA prior to any other rep...

Tbf1 and Vid22 promote resection and non-homologous end joining of DNA double-strand break ends.

The repair of DNA double-strand breaks (DSBs) is crucial for maintaining genome stability. The Saccharomyces cerevisiae protein Tbf1, which is characterized by a Myb domain and is related to mammalian TRF1 and TRF2, has been proposed to act as a transcriptional activator. Here, we show that Tbf1 and its interacting protein Vid22 are new players in the response to DSBs. Inactivation of either TB...

Non-homologous end joining as a mechanism of DNA repair

In spite of its essential role as the carrier of genetic information, DNA is not an inert structure. The genome is susceptible to potentially mutagenic threats of both endogenous and environmental origin. A dramatic threat to the covalent structure of DNA is posed by breaks in the phosphate backbone affecting one or both strands of the Watson–Crick double helix. Ionizing radiation and certain c...