作者: Madalena Tarsounas , Purificacıon Munoz , Andreas Claas , Phillip G Smiraldo , Douglas L Pittman
DOI: 10.1016/S0092-8674(04)00337-X
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摘要: Abstract The five RAD51 paralogs (RAD51B, RAD51C, RAD51D, XRCC2, and XRCC3) are required in mammalian cells for normal levels of genetic recombination resistance to DNA-damaging agents. We report here that RAD51D is also involved telomere maintenance. Using immunofluorescence labeling, electron microscopy, chromatin immunoprecipitation assays, was shown localize the telomeres both meiotic somatic cells. Telomerase-positive Rad51d −/− Trp53 primary mouse embryonic fibroblasts (MEFs) exhibited telomeric DNA repeat shortening compared or wild-type MEFs. Moreover, elevated chromosomal aberrations were detected, including end-to-end fusions, a signature dysfunction. Inhibition synthesis telomerase-negative immortalized human by siRNA resulted erosion chromosome fusion. conclude plays dual cellular role repair double-strand breaks protection against attrition