The ter (teratoma, chromosome 18) mutation causes a deficiency in primordial germ cells (PGCs) of ter/ter embryos from ter congenic mouse strains at around 8.0 days post coitum (dpc). Our previous studies indicated that in vivo, apoptosis of PGCs was caused by ter/ter gonadal somatic cells. To examine survival and proliferation in ter/ter PGCs and the deficiency caused by ter/ter gonadal somatic cells in vitro, we performed “exchange-co-culture” of PGCs and gonadal somatic cells by combining different tergenotypes, on Sl/Sl4-m220 feeder cells. The number of PGCs after 3 days culture of 9.5 dpc ter/ter PGCs with / 12.5 dpc gonadal somatic cells increased similar to that of /ter or / PGCs. The numbers of PGCs after 12 hr culture of / and ter/ter 11.5 dpc PGCs with 11.5 dpc ter/ter gonadal somatic cells decreased significantly when compared to those cultured with / somatic cells. PGCs preferred the WT1-positive gonadal somatic cells, Sertoli cells, to the feeder cells. Both TUNEL and BrdU assays showed that ter/ter somatic cells induced apoptosis but were independent of DNA synthesis in PGCs “exchange-co-cultured”. Through these results, we demonstrated for the first time that in vitro ter/ter PGCs showed survival and proliferation activities in response to the gonadal somatic cells and that ter/ter gonadal somatic cells caused apoptosis in PGCs through cell-cell contact.