Mutant meiotic chromosome core components in mice can cause apparent sexual dimorphic endpoints at prophase or X-Y defective male-specific sterility
Mutant meiotic chromosome core components in mice can cause apparent sexual dimorphic endpoints at prophase or X-Y defective male-specific sterility
复制标题
DOI：
10.1007/s00412-005-0334-8
复制
发表时间：
2005-07-01
期刊：
影响因子：
1.6
通讯作者：
Moens, PB
中科院分区：
文献类型：
--
作者：
Kolas, NK;Marcon, E;Moens, PB
在小鼠减数分裂前期引起生殖细胞死亡的遗传修饰通常具有性二型表型，其中卵母细胞比精母细胞达到更高级的阶段。为了确定这些二态性在多大程度上是由于男性与女性减数分裂前期发育的差异，我们比较了野生型和突变型小鼠两种性别的减数分裂染色体事件。我们报告胎儿卵母细胞核的结构和重组相关蛋白的丰度和出现的时间过程。与成年睾丸中精母细胞的连续发育相比，交配后连续几天的卵母细胞显示出快速、同步的减数分裂前期发育。因此，需要2-3天的遗传缺陷，从开始的前期达到逮捕登记粗线期作为发育终点的卵母细胞。另一方面，粗线期精母细胞通常在前期开始后的4-10天内积累，这将是罕见的，这使得终点比卵母细胞更早出现。我们的结论是，这些不同的物流创建明显的性别二态性终点。对于更明显的性二态性，我们研究了小鼠减数分裂前期的减数分裂染色体核心成分的遗传修饰，导致男性，而不是女性不育。雄性不育与性染色体核心和X-Y染色质组织结构改变之间的相关性可能表明，来自XY结构域（XY染色体核心、染色质、致密体和性体）的受损信号可能会干扰精母细胞通过前期的进展。卵母细胞，在没有X-Y对的情况下，不会遭受这种缺陷。
Genetic modifications causing germ cell death during meiotic prophase in the mouse frequently have sexually dimorphic phenotypes where oocytes reach more advanced stages than spermatocytes. To determine to what extent these dimorphisms are due to differences in male versus female meiotic prophase development, we compared meiotic chromosome events in the two sexes in both wild-type and mutant mice. We report the abundance and time course of appearance of structural and recombination-related proteins of fetal oocyte nuclei. Oocytes at successive days post coitus show rapid, synchronous meiotic prophase development compared with the continuous spermatocyte development in adult testis. Consequently, a genetic defect requiring 2-3 days from the onset of prophase to reach arrest registers pachytene as the developmental endpoint in oocytes. Pachytene spermatocytes, on the other hand, which normally accumulate during days 4-10 after the onset of prophase, will be rare, giving the appearance of an earlier endpoint than in oocytes. We conclude that these different logistics create apparent sexually dimorphic endpoints. For more pronounced sexual dimorphisms, we examined meiotic prophase of mice with genetic modifications of meiotic chromosome core components that cause male but not female sterility. The correlations between male sterility and alterations in the organization of the sex chromosome cores and X-Y chromatin may indicate that impaired signals from the XY domain (XY chromosome cores, chromatin, dense body and sex body) may interfere with the progression of the spermatocyte through prophase. Oocytes, in the absence of the X-Y pair, do not suffer such defects.