Fanconi anemia (FA) is a complex recessive genetic disease that causes bone marrow
failure in children. The mechanism by which the gene for FA group C (Fancc) impinges on
the normal hematopoietic program is unknown. Here we demonstrate that the bone marrow
from Fancc−/− mice have reduced ability for primary and secondary long-term reconstitution
of myeloablated recipients compared to wild-type or heterozygous mice, indicating that the
Fancc gene product is required for the maintenance of normal numbers of hematopoietic …