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oai:repisalud.isciii.es:20.500.12105/261702025-12-18T12:56:19Zcom_20.500.12105_2273com_20.500.12105_2202col_20.500.12105_19571

00925njm 22002777a 4500 dc Espejel, Silvia author Franco, Sonia author Rodriguez Perales, Sandra author Bouffler, Simon D author Cigudosa, Juan C author Blasco, MA author 2002-05-01 Here we analyze the functional interaction between Ku86 and telomerase at the mammalian telomere by studying mice deficient for both proteins. We show that absence of Ku86 prevents the end-to-end chromosomal fusions that result from critical telomere shortening in telomerase-deficient mice. In addition, Ku86 deficiency rescues the male early germ cell apoptosis triggered by short telomeres in these mice. Together, these findings define a role for Ku86 in mediating chromosomal instability and apoptosis triggered by short telomeres. In addition, we show here that Ku86 deficiency results in telomerase-dependent telomere elongation and in the fusion of random pairs of chromosomes in telomerase-proficient cells, suggesting a model in which Ku86 keeps normal-length telomeres less accessible to telomerase-mediated telomere lengthening and to DNA repair activities. EMBO J . 2002 May 1;21(9):2207-19. EMBO JOURNAL 11980718 https://hdl.handle.net/20.500.12105/26170 Mammalian Ku86 mediates chromosomal fusions and apoptosis caused by critically short telomeres.