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 Blood, 15 December 2004, Vol. 104, No. 13, pp. 3927-3935.
Prepublished online as a Blood First Edition Paper on August 19, 2004; DOI 10.1182/blood-2003-10-3626.

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HEMATOPOIESIS

Telomere dynamics in Fancg-deficient mouse and human cells

Sonia Franco, Henri J. van de Vrugt, Piedad Fernández, Miguel Aracil, Fre Arwert, and María A. Blasco

From the Molecular Oncology Program, Spanish National Cancer Centre (CNIO), Madrid, Spain; Department of Clinical Genetics and Human Genetics, VU University Medical Center, Amsterdam, The Netherlands; and Department of Immunology and Oncology (DIO), National Center of Biotechnology (CNBCSIC), Campus de Cantoblanco, Madrid, Spain.

A number of DNA repair proteins also play roles in telomere metabolism. To investigate whether the accelerated telomere shortening reported in Fanconi anemia (FA) hematopoietic cells relates to a direct role of the FA pathway in telomere maintenance, we have analyzed telomere dynamics in Fancg-deficient mouse and human cells. We show here that both hematopoietic (stem and differentiated bone marrow cells, B and T lymphocytes) and nonhematopoietic (germ cells, mouse embryonic fibroblasts [MEFs]) Fancg-/- mouse cells display normal telomere length, normal telomerase activity, and normal chromosome end-capping, even in the presence of extensive clastogen-induced cytogenetic instability (mitomycin C [MMC], gamma-radiation). In addition, telomerase-deficient MEFs with humanlike telomere length and decreased Fancg expression (G5 Terc-/-/Fancg shRNA3 MEFs) display normal telomere maintenance. Finally, early-passage primary fibroblasts from patients with FA of complementation group G as well as primary human cells with reduced FANCG expression (FANCG shRNA IMR90 cells) show no signs of telomere dysfunction. Our observations indicate that accelerated telomere shortening in patients with FA is not due to a role of FANCG at telomeres but instead may be secondary to the disease. These findings suggest that telomerase-based therapies could be useful prophylactic agents in FA aplastic anemia by preserving their telomere reserve in the context of the disease. (Blood. 2004;104:3927-3935)


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