Late onset of spermatogenesis and gain of fertility in POG-deficient mice indicate that POG is not necessary for the proliferation of spermatogonial
Late onset of spermatogenesis and gain of fertility in POG-deficient mice indicate that POG is not necessary for the proliferation of spermatogonial
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DOI：
10.1095/biolreprod.102.014654
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发表时间：
2003-07-01
影响因子：
3.6
通讯作者：
Bishop, CE
中科院分区：
文献类型：
--
作者：
Lu, B;Bishop, CE
生殖细胞缺陷（gcd）小鼠突变是一种隐性的转基因插入突变，与两个Chr 11基因Pog（生殖细胞增殖）和Vrk 2（牛痘病毒相关蛋白激酶2）的破坏有关。我们最近发现，像gcd/gcd小鼠一样，靶向Pog（-/-）雄性和雌性在4-6周龄时几乎没有精子发生或卵子发生。因为在gcd/gcd和Pog（-1-）小鼠中Pog缺失，所以比较两种小鼠模型的表型是适当的。在这里，我们报告，不像POG缺陷的女性，生殖细胞在POG缺陷的男性最终填充曲细精管在9周，生育能力可以达到12周。纯合子gcd/gcd男性没有表现出类似程度的生殖细胞群体，大多数gcd/gcd男性在16和22周龄时仍然不育。比较Pog（-/-）和gcd/gcd雄性动物在产后13.5天和产后1天的生殖细胞缺乏程度，发现在两个时间点，gcd/gcd雄性动物的生殖细胞远少于Pog-1-雄性动物。我们的数据表明，Pog是必要的适当的原始生殖细胞增殖在胚胎阶段，但出生后的精原细胞增殖是不需要的。因此，成年Pog（-/-）和gcd/gcd小鼠的精子发生潜力的差异可能是由于生殖细胞缺乏的严重性，而不是由于gcd/gcd精原细胞不能有效地增殖。与Pog（-/-）小鼠相比，在gcd/gcd雄性中观察到的精子发生开始前生殖细胞的更大缺陷表明不同的背景影响Pog缺失的结果，或者Vrk 2对生殖细胞发育具有额外的影响。
The germ cell-deficient (gcd) mouse mutation is a recessive, transgenic insertional mutation associated with the disruption of two Chr11 genes, Pog (proliferation of germ cells) and Vrk2 (vaccinia virus-related protein kinase 2). We have recently shown that like gcd/gcd mice, targeted Pog(-/-) males and females show virtually no spermatogenesis or oogenesis at 4-6 wk of age. Because Pog is deleted in gcd/gcd and Pog(-1-) mice, a comparison of the phenotypes of the two mouse models is appropriate. Here, we report that unlike in POG-deficient females, the germ cells in POG-deficient males eventually populate the seminiferous tubules at 9 wk, and fertility can be achieved by 12 wk. Homozygous gcd/gcd males did not show a similar degree of germ cell population, and most gcd/gcd males remained infertile at 16 and 22 wk of age. A comparison of the degree of germ cell deficiency at 13.5 days postcoitum and 1 day postpartum between Pog(-/-) and gcd/gcd males revealed that gcd/gcd males had far fewer germ cells than Pog-1- males at both time points. Our data suggest that Pog is essential for proper primordial germ cell proliferation in the embryonic stage but is not needed for spermatogonial proliferation after birth. Thus, the difference in the spermatogenetic potential in adult Pog(-/-) and gcd/gcd mice may result from the severity of germ cell deficiency rather than from the inability of gcd/gcd spermatogonia to proliferate efficiently. The greater deficiency of germ cells before the onset of spermatogenesis seen in gcd/gcd males compared to Pog(-/-) mice suggests either that the different background affects the outcome of Pog deletion or that Vrk2 has additional effects on germ cell development.