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Molecular and Cellular Biology, June 2001, p. 3642-3651, Vol. 21, No. 11
Department of Immunology and Oncology, Centro
Nacional de Biotecnología, Madrid E-28049,
Spain,1 and Department of Microbiology,
Boston University School of Medicine, Boston, Massachusetts
02118-25262
Received 2 November 2000/Returned for modification 11 December
2000/Accepted 23 February 2001
The major pathway in mammalian cells for repairing DNA
double-strand breaks (DSB) is via nonhomologous end joining. Five
components function in this pathway, of which three (Ku70, Ku80, and
the DNA-dependent protein kinase catalytic subunit [DNA-PKcs])
constitute a complex termed DNA-dependent protein kinase (DNA-PK).
Mammalian Ku proteins bind to DSB and recruit DNA-PKcs to the break.
Interestingly, besides their role in DSB repair, Ku proteins bind to
chromosome ends, or telomeres, protecting them from end-to-end fusions.
Here we show that DNA-PKcs
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.11.3642-3651.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
The Absence of the DNA-Dependent Protein Kinase
Catalytic Subunit in Mice Results in Anaphase Bridges and in Increased
Telomeric Fusions with Normal Telomere Length and G-Strand
Overhang
/
cells display an increased
frequency of spontaneous telomeric fusions and anaphase bridges.
However, DNA-PKcs deficiency does not result in significant changes in
telomere length or in deregulation of the G-strand overhang at the
telomeres. Although less severe, this phenotype is reminiscent of the
one recently described for Ku86-defective cells. Here we show that,
besides DNA repair, a role for DNA-PKcs is to protect telomeres, which
in turn are essential for chromosomal stability.
*
Corresponding author. Mailing address: Department of
Immunology and Oncology, Centro Nacional de Biotecnología,
Madrid E-28049, Spain. Phone: 34-915854846. Fax: 34-913720493. E-mail:
mblasco{at}cnb.uam.es.
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