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2004 Scientific Report

tery and enter the

tery and enter the genital ridge, where they collaborate with the somatic gonad cells to form the gonads. The PGCs proliferate during their migration. We are studying the spontaneous mutation atrichosis (at), which causes male and female sterility. Preliminary data suggest that this mutation affects fetal germ cell proliferation. We found that by 12.5 dpc, there already are significantly fewer germ cells in the gonads of atrichosis embryos relative to the wild type. We have mapped the atrichosis mutation to a 270-kb region on chromosome 10. We are now screening the candidate genes by transgenic rescue and direct sequencing. Another mutation we are studying is in the sks gene; this mutation affects normal meiosis in both sexes. Our results indicate that sks is required for the metaphase/anaphase transition in meiosis I. In the sks mutant, homologous chromosomes fail to separate; therefore, meiosis is stopped at MI. We have demonstrated that this failure is due to the inability of the sks mutant to degrade securin in the primary spermatocytes and possibly in the oocytes. Recent Publications Mustonen, Tuija, Mark Tummers, Tadahisa Mikami, Nobuyuki Ito, Nian Zhang, Thomas Gridley, and Irma Thesleff. 2002. Lunatic fringe, FGF, and BMP regulate the Notch pathway during epithelial morphogenesis of teeth. Developmental Biology 248(2): 281–293. Zhang, Nian, Christine R. Norton, and Thomas Gridley. 2002. Segmentation defects of Notch pathway mutants and absence of a synergistic phenotype in lunatic fringe/radical fringe double mutant mice. Genesis 33(1): 21–28. From left to right: Kong, Zhang, Kang, Chen 66

Daniel Nathans Memorial Award

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