Sakurai Takayuki, Iguchi Taisen, Moriwaki Kazuo, Noguchi Motoko
Graduate School of Integrated Science, Yokohama City University, Yokohama 236, Japan.
Department of Biology, Faculty of Science, Shizuoka University, Ohya 836, Shizuoka 422, Japan.
Dev Growth Differ. 1995 Jun;37(3):293-302. doi: 10.1046/j.1440-169X.1995.t01-2-00007.x.
The ter (teratoma) mutation causes primordial germ cell (PGC) deficiency in ter/ter embryos at 9.5-12.5 days of post-coitum (dpc) in mouse strains 129/Sv-ter and LTXBJ-ter. To study the effects of the ter mutation on the PGC development more precisely, we examined the PGC number and distribution in 7.5-12.5 dpc embryo of ter congenic C57BL/6J-ter strain using their complete serial sections. The ter genotypes of embryos were identified by the polymerase chain reaction (PCR) polymorphisms of the microsatellite DNA of the Grl-1 locus mapped near the ter locus. Results showed that: (i) the PGC number in ter/ter embryos was similar to those of + /ter and + / + embryos at 7.5 dpc, and did not increase at 8.0-12.5 dpc, although those of normal littermates did usually; (ii) the PGC migration to genital ridges was never affected in all embryos; and (iii) the ter genotype difference in the PGC numbers was not recognized between + /ter and + / + embryos. We concluded that the ter mutation does not affect the PGC appearance around 7.5 dpc, but first causes PGC deficiency around 8.0 dpc at the beginning of their migration and proliferation, suggesting that the normal function of the ter gene may be essential for the proliferation or survival mechanisms of PGC.
在129/Sv-ter和LTXBJ-ter小鼠品系中,ter(畸胎瘤)突变会导致交配后9.5 - 12.5天(dpc)的ter/ter胚胎中原始生殖细胞(PGC)缺乏。为了更精确地研究ter突变对PGC发育的影响,我们使用ter同基因C57BL/6J-ter品系7.5 - 12.5 dpc胚胎的完整连续切片,检查了PGC的数量和分布。通过位于ter基因座附近的Grl-1基因座微卫星DNA的聚合酶链反应(PCR)多态性来鉴定胚胎的ter基因型。结果显示:(i)在7.5 dpc时,ter/ter胚胎中的PGC数量与 + /ter和 + / +胚胎相似,并且在8.0 - 12.5 dpc时没有增加,而正常同窝小鼠的PGC数量通常会增加;(ii)所有胚胎中PGC向生殖嵴的迁移从未受到影响;(iii)在 + /ter和 + / +胚胎之间未发现PGC数量上的ter基因型差异。我们得出结论,ter突变在7.5 dpc左右不影响PGC的出现,但在8.0 dpc左右PGC开始迁移和增殖时首先导致PGC缺乏,这表明ter基因的正常功能可能对PGC的增殖或存活机制至关重要。