The importance of XRCC2 in RAD51-related DNA damage repair |
| |
| Authors: | Cathryn E. Tambini Karen G. Spink Caroline J. Ross Mark A. Hill John Thacker |
| |
| Affiliation: | 1. Department of Cell and Molecular Biology, University of Rhode Island, 120 Flagg Road, Kingston, RI 02881, United States;2. Dana-Farber Cancer Institute/Boston Children''s Cancer and Blood Disorders Center, Boston, MA 02215, United States;1. Biomedical Science Program, Graduate School, Khon Kaen University, Khon Kaen, Thailand;2. Centre for Research and Development of Medical Diagnostic Laboratories, Faculty of Associated Medical Sciences, Khon Kaen University, Khon Kaen, Thailand;3. Department of Medical Genetics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China;1. Trent University, Canada;2. Carleton University, Canada;1. Prenatal Diagnostic Center, Dongguan Maternal & Children Health Hospital, Dongguan, Guangdong Province, People''s Republic of China;2. Prenatal Diagnostic Center, Guangzhou Women & Children Medical Center, Guangzhou Medical College, Guangzhou, Guangdong Province, People''s Republic of China;3. Department of Medical Genetics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong Province, People''s Republic of China |
| |
| Abstract: | The repair of DNA damage by homologous recombination (HR) is a key pathway for the maintenance of genetic stability in mammalian cells, especially during and following DNA replication. The central HR protein is RAD51, which ensures high fidelity DNA repair by facilitating strand exchange between damaged and undamaged homologous DNA segments. Several RAD51-like proteins, including XRCC2, appear to help with this process, but their roles are not well understood. Here we show that XRCC2 is highly conserved and that most substantial truncations of the protein destroy its ability to function. XRCC2 and its partner protein RAD51L3 are found to interact with RAD51 in the 2-hybrid system, and XRCC2 is shown to be important but not essential for the accumulation of RAD51 at the sites of DNA damage. We visualize the localization of XRCC2 protein at the same sites of DNA damage for the first time using specialized irradiation conditions. Our data indicate that an important function of XRCC2 is to enhance the activity of RAD51, so that the loss of XRCC2 results in a severe delay in the early response of RAD51 to DNA damage. |
| |
| Keywords: | |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
