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Telomere shortening has been linked to rare human disorders that present with bone marrow failure including Fanconi anemia (FA).  FANCC  is one of the most commonly mutated FA genes in FA patients and the  FANCC  subtype tends to have a relatively early onset of bone marrow failure and hematologic malignancies. Here, we studied the role of Fancc in telomere length regulation in mice. Deletion of  Fancc  ( Fancc  −/− ) did not affect telomerase activity, telomere length or telomeric end-capping in a mouse strain possessing intrinsically long telomeres. However, ablation of Fancc did exacerbate telomere attrition when murine bone marrow cells experienced high cell turnover after serial transplantation. When  Fancc  −/−  mice were crossed into a telomerase reverse transcriptase heterozygous or null background ( Tert  +/−  or  Tert  −/− ) with short telomeres,  Fancc  deficiency led to an increase in the incidence of telomere sister chromatid exchange. In contrast, these phenotypes were not observed in  Tert  mutant mice with long telomeres. Our data indicate that  Fancc  deficiency accelerates telomere shortening during high turnover of hematopoietic cells and promotes telomere recombination initiated by short telomeres.

FANCC suppresses short telomere-initiated telomere sister chromatid exchange