DEVELOPMENTAL BIOLOGICAL STUDIES ON FUNCTION OF THE ter GENEIN DEFICIENCY AND TERATOCARCINOGENESIS OF PRIMORDIAL GERM CELLS IN ter MUTANT MICE

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1. The ter (teratoma) mutation caused germ cell deficiency from fetal stages to adulthood in ter/ter mice of the strain 129/Sv-ter and the ter-congenic strains, C57BL/6J-ter(B6-ter), LTXBJ-ter, and C3H/HeJ-ter (C3H-ter) which we have established by introducing the ter gene from 129/Sv-ter mice onto the genetic backgrounds of B6, LTXBJ,and C3H strains, respsctively. The ter gene induced also a high incidence of spontaneous testicular teratomas in the genetic background of 129/Sv-ter, but not experimental testicular nor ovarian teratomas in ter congenic strains.2. It was found that the ter locus maps closely to Grl-1 locus on Chr. 18 and that cach ter genotype of each embryo or adult can be identified by SSLP (Simple Sequence Length Polymorphisms) of the microsatellite DNA of the Grl-1 gene.3. By histochemical studies on ter congenic embryos ter-genotyped by SSLP,it was showed that the ter gene first causes primordial germ cell deficiency in ter mutant embryos at 8 days of gestation.4. Germ cell deficiency occurred in testes reconstituted from reaggregates produced from+/+and+/ter gonocytes and ter/ter somatic cells from dissociated fetal testes in the ter congenic strain, whereas spermatogenesis did in those from normal gonocytes and somatic cells, suggesting that the ter gene may cause germ cell deficiency by affecting somatic cells in fetal ter/ter testes.5. Testicular teratomas were induced in fetal testes reconstituted between LTXBJ gonocytes and 129/Sv-ter somatic cells, whereas no tumors were in those recombined reciprocally, showing that somatic cells from fetal testes having 129/Sv-ter genetic background may play a key role in testicular teratocarcinogenesis.