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Human Molecular Genetics, 2002, Vol. 11, No. 25 3135-3144
© 2002 Oxford University Press

The Bloom syndrome helicase BLM interacts with TRF2 in ALT cells and promotes telomeric DNA synthesis

Dimitrios J. Stavropoulos1,2, Paul S. Bradshaw1,2, Xiaobin Li2, Ivan Pasic1,2, Kevin Truong3,4, Mitsuhiko Ikura3,4, Mark Ungrin3 and M. Stephen Meyn1,2,5,*

1Department of Molecular and Medical Genetics, University of Toronto, Toronto, Canada M5S 1A8, 2Genetics and Genomic Biology Program, Hospital for Sick Children, Toronto, Canada M5G 1X8, 3Department of Medical Biophysics, University of Toronto, Toronto, Canada M5G 2M9, 4Division of Molecular and Structural Biology, Ontario Cancer Institute, Toronto, Canada M5G 2M9 and 5Department of Pediatrics, University of Toronto, Toronto, Canada M5G 1X8

Received July 26, 2002; Accepted October 7, 2002

Telomerase-negative immortalized human cells maintain telomeres by alternative lengthening of telomeres (ALT) pathway(s), which may involve homologous recombination. We find that endogenous BLM protein co-localizes with telomeric foci in ALT human cells but not telomerase positive immortal cell lines or primary cells. BLM interacts in vivo with the telomeric protein TRF2 in ALT cells, as detected by FRET and co-immunoprecipitation. Transient over-expression of green fluorescent protein (GFP)-BLM results in marked, ALT cell-specific increases in telomeric DNA. The association of BLM with telomeres and its effect on telomere DNA synthesis require a functional helicase domain. Our results identify BLM as the first protein found to affect telomeric DNA synthesis exclusively in human ALT cells and suggest that BLM facilitates recombination-driven amplification of telomeres in ALT cells.

* To whom correspondence should be addressed at: Genetics and Genome Biology Program, Hospital for Sick Children, 11-101 Elm Wing, Toronto, 555 University Ave, Toronto, Canada M5G 1X8. Tel: +1 4168138485; Fax: +1 4168134931; Email: meyn{at}sickkids.ca


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