MAPPING AND DEVELOPMENTAL BIOTECHNOLOGY OF THE ter GENE RESPONSIBLE FOR GERM CELL DEFICIENCY IN MICE.

我们从129/Sv-ter小鼠中引入ter基因，在C57BL/6J和LTXBJ菌株的遗传背景上建立了ter（畸胎瘤）基因，并在129/Sv-ter小鼠中建立了C57BL/6J和LTXBJ-ter。定位和发育生物技术方法，如重组睾丸，是研究ter基因诱导的不育机制的有用工具，概述如下1。对LTXBJ-ter菌株中每个胚胎中被认为是原始生殖细胞（PGCs）的碱性磷酸酶阳性细胞的计数表明，ter基因导致LTXBJ-ter菌株中迁移阶段的PGCs缺乏，而+/+和+/ter菌株中PGCs的增殖与LTXBJ菌株一样2。在129/ v-ter（+/+）小鼠睾丸畸胎瘤易感小鼠中，由分离后肠和胎儿睾丸的PGCs和体细胞重组的睾丸中，来自后肠的PGCs分化为正常配子和畸胎瘤，这表明重组睾丸也可以作为分析PGC迁移阶段ter基因功能的有用工具。3 .利用C57BL/6J-ter （+/ter）小鼠和多个近交系进行ter基因与32个遗传标记的连锁试验，结果表明ter基因与小鼠18号染色体上Grl-1位点定位密切，并可通过Grl-1基因的PCR多态性鉴定胚胎或成体的ter基因型。LTXBJ-ter分离胚胎睾丸，生殖细胞（+/+和+/ter）与体细胞（+/+和+/ter）或（ter/ter）重新聚集。前一种组合的重聚集体重建正常睾丸，后一种组合的重聚集体重建生殖细胞缺陷睾丸。提示ter基因在睾丸体细胞上表达，由此产生的未知缺陷反过来诱发生殖细胞缺陷。

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.