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Published 9 July 2001. doi:10.1083/jcb.200103049
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© The Rockefeller University Press, 0021-9525/2001/7/49 $5.00
The Journal of Cell Biology, Volume 154, Number 1, July 9, 2001 49-60

Article

 Normal telomere length and chromosomal end capping in poly(ADP-ribose) polymerase–deficient mice and primary cells despite increased chromosomal instability

Enrique Samper1, Fermín A. Goytisolo1, Josiane Ménissier-de Murcia2, Eva González-Suárez1, Juan C. Cigudosa3, Gilbert de Murcia2 and María A. Blasco1

1 Department of Immunology and Oncology, Centro Nacional de Biotecnología-CSIC, Campus Cantoblanco, E-28049 Madrid, Spain
2 Centre National de la Recherche Scientifique, Laboratoire Conventionné avec le Commissariat à lEnergie Atomique, Ecole Superieure de Biotechnologie de Strasbourg, 67400 Illkirch-Graffenstaden, France
3 Cytogenetics Unit, Centro Nacional de Investigaciones Oncologicas Carlos III, Majadahonda, E-28220 Madrid, Spain

Address correspondence to María Blasco, Department of Immunology and Oncology, Centro Nacional de Biotecnologia - CSIC, Campus Cantoblanco, E-28049 Madrid, Spain. Tel.: (34) 915-854-846; Fax: (34) 913-720-493. E-mail: mblasco{at}cnb.uam.es

Poly(ADP-ribose) polymerase (PARP)-1, a detector of single-strand breaks, plays a key role in the cellular response to DNA damage. PARP-1–deficient mice are hypersensitive to genotoxic agents and display genomic instability due to a DNA repair defect in the base excision repair pathway. A previous report suggested that PARP-1–deficient mice also had a severe telomeric dysfunction consisting of telomere shortening and increased end-to-end fusions (d'Adda di Fagagna, F., M.P. Hande, W.-M. Tong, P.M. Lansdorp, Z.-Q. Wang, and S.P. Jackson. 1999. Nat. Genet. 23:76–80). In contrast to that, and using a panoply of techniques, including quantitative telomeric (Q)-FISH, we did not find significant differences in telomere length between wild-type and PARP-1-/- littermate mice or PARP-1-/- primary cells. Similarly, there were no differences in the length of the G-strand overhang. Q-FISH and spectral karyotyping analyses of primary PARP-1-/- cells showed a frequency of 2 end-to-end fusions per 100 metaphases, much lower than that described previously (d'Adda di Fagagna et al., 1999). This low frequency of end-to-end fusions in PARP-1-/- primary cells is accordant with the absence of severe proliferative defects in PARP-1-/- mice. The results presented here indicate that PARP-1 does not play a major role in regulating telomere length or in telomeric end capping, and the chromosomal instability of PARP-1-/- primary cells can be explained by the repair defect associated to PARP-1 deficiency. Finally, no interaction between PARP-1 and the telomerase reverse transcriptase subunit, Tert, was found using the two-hybrid assay.

Key Words: telomeres; PARP-1; telomerase; DNA repair; chromosomal stability


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