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Nucleic Acids Research Advance Access originally published online on October 24, 2007
Nucleic Acids Research 2007 35(21):7267-7278; doi:10.1093/nar/gkm738
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Nucleic Acids Research, 2007, Vol. 35, No. 21 7267-7278
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Replication protein A prevents accumulation of single-stranded telomeric DNA in cells that use alternative lengthening of telomeres

Amra Grudic1,2, Åsne Jul-Larsen1,2, Stuart J. Haring3, Marc S. Wold3, Per Eystein Lønning1, Rolf Bjerkvig2,4 and Stig Ove Bøe1,2,*

1Section of Oncology, Department of Medicine, Haukeland University Hospital, 2Section of Anatomy and Cell Biology, Department of Biomedicine, University of Bergen, Jonas Lies vei 91, N-5009, Bergen, Norway, 3Department of Biochemistry, University of Iowa Carver College of Medicine, Iowa City, IA, 52242, USA and 4NorLux, Neuro-Oncology, Centre Recherche Public Santé, Luxembourg

*To whom correspondence should be addressed. Tel: +47 55586455; Fax: +47 55586360; Email: stig.boe{at}vir.uib.no

Received May 27, 2007. Revised August 24, 2007. Accepted September 5, 2007.

The activation of a telomere maintenance mechanism is required for cancer development in humans. While most tumors achieve this by expressing the enzyme telomerase, a fraction (5–15%) employs a recombination-based mechanism termed alternative lengthening of telomeres (ALT). Here we show that loss of the single-stranded DNA-binding protein replication protein A (RPA) in human ALT cells, but not in telomerase-positive cells, causes increased exposure of single-stranded G-rich telomeric DNA, cell cycle arrest in G2/M phase, accumulation of single-stranded telomeric DNA within ALT-associated PML bodies (APBs), and formation of telomeric aggregates at the ends of metaphase chromosomes. This study demonstrates differences between ALT cells and telomerase-positive cells in the requirement for RPA in telomere processing and implicates the ALT mechanism in tumor cells as a possible therapeutic target.


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