Fanconi anemia complementation group C is required for proliferation of murine primordial germ cells
Copyright policy )Fanconi anemia complementation group C is required for proliferation of murine primordial germ cells
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.
- University of Washington United States
- University of Mary United States
- University of Washington, University libraries United States
- Fred Hutchinson/University of Washington/Seattle Children’s Cancer Consortium United States
- Jackson Laboratory United States
Male, Cell Cycle Proteins, Fanconi-Anemia-Complementation-Group-Proteins, Inbred C57BL, P.H.S, Mice, Pregnancy, Mitotic-Index, Testis, genetics, Fanconi-Anemia-Complementation-Group-C-Protein, Mice-Mutant-Strains, DNA-Binding-Proteins, Reverse Transcriptase Polymerase Chain Reaction, Fanconi Anemia Complementation Group C Protein, Nuclear Proteins, Spermatozoa, Fanconi Anemia Complementation Group Proteins, Reverse-Transcriptase-Polymerase-Chain-Reaction, Mutant Strains, DNA-Binding Proteins, Meiosis, Female, Cell-Division, Cell Division, mice, 610, Research Support, Cell-Cycle-Proteins, 576, Embryonic and Fetal Development, Nuclear-Proteins, embryology, Mitotic Index, primordial germ cells, Animals, Ovum, Mice-Inbred-C57BL, Ovary, Proteins, Mice, Mutant Strains, Mice, Inbred C57BL, Fanconi Anemia, Fanconi anemia, Embryonic-and-Fetal-Development, Fanconi-Anemia, physiology, gene expression, cytology, Gene-Deletion, U.S. Gov't, metabolism, Gene Deletion
Male, Cell Cycle Proteins, Fanconi-Anemia-Complementation-Group-Proteins, Inbred C57BL, P.H.S, Mice, Pregnancy, Mitotic-Index, Testis, genetics, Fanconi-Anemia-Complementation-Group-C-Protein, Mice-Mutant-Strains, DNA-Binding-Proteins, Reverse Transcriptase Polymerase Chain Reaction, Fanconi Anemia Complementation Group C Protein, Nuclear Proteins, Spermatozoa, Fanconi Anemia Complementation Group Proteins, Reverse-Transcriptase-Polymerase-Chain-Reaction, Mutant Strains, DNA-Binding Proteins, Meiosis, Female, Cell-Division, Cell Division, mice, 610, Research Support, Cell-Cycle-Proteins, 576, Embryonic and Fetal Development, Nuclear-Proteins, embryology, Mitotic Index, primordial germ cells, Animals, Ovum, Mice-Inbred-C57BL, Ovary, Proteins, Mice, Mutant Strains, Mice, Inbred C57BL, Fanconi Anemia, Fanconi anemia, Embryonic-and-Fetal-Development, Fanconi-Anemia, physiology, gene expression, cytology, Gene-Deletion, U.S. Gov't, metabolism, Gene Deletion
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