Linking double-stranded DNA breaks to the recombination activating gene complex directs repair to the nonhomologous end-joining pathway.
Two major DNA repair pathways, nonhomologous end-joining (NHEJ) and homologous recombination (HR), repair double-stranded DNA breaks (DSBs) in all eukaryotes. Additionally, several alternative end-joining pathways (or subpathways) have been reported that characteristically use short-sequence homologies at the DNA ends to facilitate joining. How a cell chooses which DNA repair pathway to use (at any particular DSB) is a central and largely unanswered question. For one type of DSB, there is apparently no choice. DSBs mediated by the lymphocyte-specific recombination activating gene (RAG) endonuclease are repaired virtually exclusively by NHEJ. Here we demonstrate that non-RAG-mediated DSBs can be similarly forced into the NHEJ pathway by physical association with the RAG endonuclease.
Cui
Xiaoping
X
College of Veterinary Medicine and Department of Pathobiology and Diagnostic Investigation, Michigan State University, East Lansing, MI 48824, USA.
Meek
Katheryn
K
D034961:Antigens, Nuclear; D002470:Cell Survival; D053903:DNA Breaks, Double-Stranded; D004260:DNA Repair; D051747:DNA-Activated Protein Kinase / Q000172:deficiency; D004268:DNA-Binding Proteins / Q000172:deficiency; D018398:Homeodomain Proteins / Q000378:metabolism*; D000072200:Ku Autoantigen; D046912:Multiprotein Complexes / Q000378:metabolism; D010957:Plasmids / Q000378:metabolism; D011485:Protein Binding; D011995:Recombination, Genetic
D034961:Antigens, Nuclear; D004268:DNA-Binding Proteins; D018398:Homeodomain Proteins; D046912:Multiprotein Complexes; C064658:RAG-1 protein; D051747:DNA-Activated Protein Kinase; D000072200:Ku Autoantigen