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Fanconi anemia complementation group C is required for proliferation of murine primordial germ cells

By Jessica J. Nadler and Robert E. Braun


Fanconi anemia is a polygenic trait hypothesized to be a DNA damage repair disease. We show that all three Fanconi anemia loci that have been cloned are expressed in the embryonic gonad during the period of primordial germ cell proliferation. Mice mutant for the Fanconi anemia complementation group C locus (Fancc) have reduced germ cell numbers as early as embryonic day E12.5, suggesting the Fancc protein functions prior to meiosis in both sexes. Depletion in the mutant occurs at a time when all three loci would be expressed in a wild-type gonad, implying a function in the early germline. Determination of the mitotic index of primordial germ cells by BrdU incorporation shows that germ cells in Fancc(-/-) mice proliferate significantly more slowly than littermate controls. This study demonstrates Fancc is required for mitotic proliferation of primordial germ cells.

Topics: mice, gene expression, primordial germ cells, Fanconi anemia, Meiosis, Testis, embryology, Male, Mice, Inbred C57BL, Mitotic Index, Mice, Animals, Cell Division, Cell Cycle Proteins, Fanconi Anemia Complementation Group C Protein, Pregnancy, Nuclear Proteins, Ovary, embryology, DNA-Binding Proteins, Research Support, U.S. Gov't, P.H.S., Mice, Mutant Strains, Female, Gene Deletion, Fanconi Anemia Complementation Group Proteins, Ovum, cytology, physiology, Embryonic and Fetal Development, genetics, Spermatozoa, cytology, physiology, Fanconi Anemia, genetics, Reverse Transcriptase Polymerase Chain Reaction, Proteins, genetics, metabolism
Publisher: Wiley-Liss
Year: 2000
DOI identifier: 10.1002/1526-968x(200007)27:3<117::aid-gene40>;2-7
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