CELL BIOLOGICAL AND BIOCHEMICAL STUDIES ON FUNCTION OF THE ter GENE IN PRIMORDIAL GERM CELL DEFICIENCY IN ter MUTANT MICE.

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Mutant strains having the ter (teratoma, Chr.18) mutation can serve as useful tools for studies of proliferation, survival and teratocarcinogenesis of primordial germ cells (PGC) in mice. Characteristics of the ter gene obtained are summarized below :1.The ter gene induces PGC deficiency from 8 days of gestation in ter/ter mice of the ter-congenic strains such as B6-+/ter, LTXBJ-+/ter and 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, respectively.2.Each ter genotype of each embryo of ter-congenic strains was identified by SSLP of the microsatellite markers near the ter locus.3.PGC deficiency in ter mutant testes is ascribed to their intratubular defect and +/+ gonocytes occurred apoptosis in reconstituted testes with ter testicular somatic cells, whereas they differentiated to spermatogenic cells in those with own somatic cells. These indicate that the ter gene may function in ter somatic cells.4.This type PGC-deficiency was not rescued by addition of several PGC growth factors in vitro and was induced by apoptosis in the G1 phase of PGC.5.PGC co-cultured with own somatic cells proliferated in conditioned medium (CM) of +/+ and +/ter somatic cells of fetal gonads, but they did not in terCM.+/+CM contained protein like substance supporting PGC survival, but terCM did not. Both +/+ and ter PGC isolated proliferated on the +/+ somatic cells, but they occurred apoptosis on the ter ones.6.It is concluded that a novel PGC growth factor (designated as TER Factor, TERF), both soluble type and membrane bounded type, supporting PGC survival may be produced by gonadal somatic cells and that it may be coded by the normal gene on the ter locus, and also that ter PGC are normal.