| Project/Area Number |
11480223
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Developmental biology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
NAKATSUJI Norio Kyoto University, Institute for Frontier Medical Sciences, Professor, 再生医科学研究所, 教授 (80237312)
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| Co-Investigator(Kenkyū-buntansha) |
SAITO Tetsuichiro Kyoto University, Institute for Frontier Medical Sciences, Associate Professor, 再生医科学研究所, 助教授 (00202078)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥15,100,000 (Direct Cost: ¥15,100,000)
Fiscal Year 2001: ¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2000: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1999: ¥7,400,000 (Direct Cost: ¥7,400,000)
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| Keywords | Primordial germ cells / mouse embryo / meiosis / sex defferentiation / testis / ovary / oocytes / cell death / 遺伝子発現 / 転写因子 |
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| Research Abstract |
Mouse primordial germ cells (PGCs) migrate from the base of allantois to the genital ridge. They proliferate during the migration and after the arrival until initiation of the sex-differentiation of fetal gonads. Then, PGCs enter into the prophase of the first meiotic division in the ovary to become oocytes, while those in the testis become mitotically arrested to become prospermatogonia. Growth regulation of mouse PGCs has been studied by culturing them on feeder cells. They show a limited period of proliferation in vitro and go into the growth arrest. In the presence of multiple growth signals, however, PGCs can restart rapid proliferation and transform into the pluripotent embryonic germ (EG) cells. We developed a two-dimensional culture system in which we examined transition from the mitotic PGCs into the leptotene stage of the first meiotic division by using the meiosis-specific markers, Scp3 and Dmcl. Such entry into meiosis seems to be programmed in PGCs before reaching the genital ridges and unless inhibited by putative signals from the testicular somatic cells. In such culture system, addition of the leukemia inhibitory factor (LIF) and related ligands caused a strong suppression of the Scp3 expression and meiotic entry by PGCs, indicating that the gp130-mediated signaling may be involved in such inhibition.
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