| Project/Area Number |
18570211
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | National Institute of Genetics |
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Principal Investigator |
ASAOKA Miho National Institute of Genetics, Department of Developmental Genetics, Assistant Professor (40370118)
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| Co-Investigator(Kenkyū-buntansha) |
HIROMI Yasushi National Institute of Genetics, Department of Developmental Genetics, Professor (70291888)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,110,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | stem cells / stem cell niche / germ cells / Drosophila / ovary / primordial germ cell |
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| Research Abstract |
Stem cells in the adult tissue are maintained by a special microenvironment called "niche", which produces signals that maintain stem cell specification and function. However, how stem-cell fate and niche-cell fate are initially established during organogenesis is largely unknown. We have studied regulation mechanisms underlying stem-cell and niche-cell fate determination using Drosophila ovary as a model system. In the Drosophila ovary, germline stem cells (GSCs) and niche cells are formed by larval-pupal transition from a subset of primordial germ cells (PGCs) and somatic cells in the ovary, respectively. Previous our lineage analysis of primordial germ cell showed that PGCs in the anterior half of the embryonic gonad frequently acquired contact with nascent niche cells in the late larval ovary and gave rise to GSCs in the adult ovary. This suggests that the GSC fate is predetermined before larval-pupal transition, possibly in the embryonic gonads, Expression of a niche-cell specific enhancer-trap marker suggested that niche cells may originate from anterior portion of embryonic somatic gonads. Here, we screened out one novel gene which is expressed somatic gonadal precursors contacting the PGCs in the anterior half of the gonads and encode a transmembrane protein. Gene knock-down in the embryonic SGPs and its null mutation resulted in the absence or decrease of GSCs in the adult ovaries. These results suggest that GSC fate determination involves SGP/PGC interaction in the anterior half of the embryonic gonad. We also screened out three candidate genes which are involved in niche cell formation and/or differentiation.
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