Mammalian Ku86 mediates chromosomal fusions and apoptosis caused by critically short telomeres

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 addit...

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Bibliographic Details
Published in:The EMBO journal 2002-05, Vol.21 (9), p.2207-2219
Main Authors: Espejel, Silvia, Franco, Sonia, Rodríguez-Perales, Sandra, Bouffler, Simon D., Cigudosa, Juan C., Blasco, María A.
Format: Article
Language:English
Subjects:
Animals
Antigens, Nuclear
apoptosis
Apoptosis - physiology
Chromosome Aberrations
Chromosomes
Chromosomes - metabolism
DNA Helicases
DNA-Binding Proteins - deficiency
DNA-Binding Proteins - metabolism
DNA-Binding Proteins - physiology
EMBO13
Ku Autoantigen
Ku86
Ku86 protein
Male
Mammals
Mice
Mice, Knockout
Nuclear Proteins - deficiency
Nuclear Proteins - physiology
Spermatozoa - physiology
telomerase
Telomerase - deficiency
Telomerase - physiology
Telomere - metabolism
Telomere - physiology
telomere dysfunction
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Summary: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.
ISSN:0261-4189
1460-2075
1460-2075
DOI:10.1093/emboj/21.9.2207