1992 Fiscal Year Final Research Report Summary
MAPPING AND DEVELOPMENTAL BIOTECHNOLOGY OF THE ter GENE RESPONSIBLE FOR GERM CELL DEFICIENCY IN MICE.
| Project/Area Number |
03680037
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory animal science
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| Research Institution | SHIZUOKA UNIVERSITY |
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Principal Investigator |
NOGUCHI Motoko SHIZUOKA UNIVERSITY, FACULTY OF SCIENCE, ASSOCIATE PROFESSOR, 理学部, 助教授 (40021951)
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| Project Period (FY) |
1991 – 1992
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| Keywords | The ter(teratoma) gene / Sterility / Germ cell deficiency / Primordial germ cell / Reconstituted testis / Mouse / Gene mapping / Developmental biotechnology |
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| Research Abstract |
The ter (teratoma) gene causes germ cell deficiency in 129/Sv-ter strain of mouse and the ter-congenic strains, C57BL/6J-ter and LTXBJ-ter which we established by introduction of the ter gene from 129/Sv-ter mice onto the genetic background of C57BL/6J and LTXBJ strains.
Mapping and developmental biotechnological method such as reconstituted testes served as useful tools in studies on the mechanism of sterility induced by the ter gene as summarized below.
1. Counts of Alkaline phosphatase positive cells considered to be primordial germ cells (PGCs) per embryo showed that the ter gene causes deficiency of PGCs in their migration stages in ter/ter fetuses in LTXBJ-ter strain, whereas PGCs in +/+ and +/ter fetuses proliferate as well as those in LTXBJ strain.
2. In testes reconstituted from reaggregates of PGCs and somatic cells from dissociated hindgut and fetal testes in 129/Sv-ter(+/+) mice that is susceptible to testicular teratomas, PGCs from hindgut differentiated to normal gametes and teratomas, suggesting that reconstituted testes can also serve as useful tools in analysis of the ter gene function in PGC migration stages.
3. The linkage tests performed between the ter gene and 32 genetic markers using C57BL/6J-ter (+/ter) mice and several inbred strains showed that the ter gene maps closely to Grl-1 locus on mouse Chromosome 18 and that the ter genotype of each embryo or adult can be identified by PCR polymorphisms of the Grl-1 gene.
4. Fetal testes in LTXBJ-ter strain were dissociated and germ cells (+/+ and +/ter) were reaggregated with somatic cells (+/+ and +/ter) or (ter/ter). Grafts of reaggregate in the former combination reconstituted normal testes, but those in the latter combination did germ cell deficient testes. It is suggested that the ter gene is expressed on testicular somatic cells and resultant but unknown defect induces in turn germ cell deficiency.
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