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doi: 10.1242/10.1242/dev.00392
DEVELOPMENT AND DISEASE |
1 Department of Molecular Cell Biology, Research Institute for Microbial
Diseases, Osaka University, Osaka 565-0871, Japan
2 Department of Biochemistry, Akita University School of Medicine, Akita
010-8543, Japan
3 Department of Laboratory Sciences for Animal Experimentation, Research
Institute for Microbial Diseases, Osaka University, Osaka 565-0871,
Japan
4 Samuel Lunenfeld Research Institute, Toronto, Ontario M5G 1X5, Canada
5 Amgen Research Institute, Ontario Cancer Institute, and University of Toronto,
Toronto, Ontario M5G 2C1, Canada
* Author for correspondenc (e-mail: tnakano{at}biken.osaka-u.ac.jp)
Accepted 14 January 2003
The tumor suppressor gene PTEN, which is frequently mutated in human cancers, encodes a lipid phosphatase for phosphatidylinositol 3,4,5-triphosphate [PtdIns(3,4,5)P3] and antagonizes phosphatidylinositol 3 kinase. Primordial germ cells (PGCs), which are the embryonic precursors of gametes, are the source of testicular teratoma. To elucidate the intracellular signaling mechanisms that underlie germ cell differentiation and proliferation, we have generated mice with a PGC-specific deletion of the Pten gene. Male mice that lacked PTEN exhibited bilateral testicular teratoma, which resulted from impaired mitotic arrest and outgrowth of cells with immature characters. Experiments with PTEN-null PGCs in culture revealed that these cells had greater proliferative capacity and enhanced pluripotent embryonic germ (EG) cell colony formation. PTEN appears to be essential for germ cell differentiation and an important factor in testicular germ cell tumor formation.
Key words: PTEN, Germ cells, Teratoma, EG cells, Mouse, Human
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