Taketo-Hosotani T, Nishioka Y, Nagamine C M, Villalpando I, Merchant-Larios H
Urology Research Laboratory, McGill University, Royal Victoria Hospital, Montreal, Canada.
Development. 1989 Sep;107(1):95-105. doi: 10.1242/dev.107.1.95.
When the Y chromosome of Mus musculus domesticus (YDOM) was introduced onto the C57BL/6 (B6) mouse background, half of the XY progeny (B6.YDOM) developed bilateral ovaries and female internal and external genitalia. We examined the fertility of the B6.YDOM sex-reversed female mouse. The chromosomal sex of the individual mouse was identified by dot hybridization with mouse Y chromosome-specific DNA probes. The results indicated that all XY females lacked regular estrous cyclicity although most were able to mate and ovulate after treatment with gonadotropins. When they had been ovariectomized and grafted with ovaries from the XX female litter mate, they initiated estrous cyclicity. Reciprocally, the XX female that had received XY ovarian grafts did not resume estrous cyclicity. Development of the XY ovary was morphologically comparable to the XX ovary until 16 day of gestation (d.g.), when most germ cells had reached the zygotene or pachytene stage of meiotic prophase. However, by the day of delivery (19 or 20 d.g.), no oocyte remained in the medullary cords of the XY ovary. In the control XX ovary, the first generation of follicles developed in the medullary region, and 5 delta-3 beta-hydroxysteroid dehydrogenase (3 beta-HSDH) activity appeared first in the stromal cells around growing follicles by 10 days after birth. In contrast, in the XY ovary, follicles were not formed in the medullary region, and 3 beta-HSDH activity appeared in epithelial cells of the oocyte-free medullary cords. Primordial follicles in the cortex region continued development in both the XX and XY ovaries. These results suggest that the XY female is infertile due to a defect inside the XY ovary. The prenatal loss of oocytes in the medullary cords may be a key event leading to abnormal endocrine function, and thereby, the absence of estrous cyclicity.
当小家鼠（YDOM）的Y染色体被导入C57BL/6（B6）小鼠背景时，一半的XY后代（B6.YDOM）发育出双侧卵巢以及雌性的内外生殖器。我们检测了B6.YDOM性反转雌性小鼠的生育能力。通过与小鼠Y染色体特异性DNA探针进行点杂交来鉴定单个小鼠的染色体性别。结果表明，所有XY雌性小鼠均缺乏规律的发情周期，尽管大多数在促性腺激素处理后能够交配和排卵。当它们被切除卵巢并移植来自XX雌性同窝仔鼠的卵巢后，它们开始出现发情周期。相反，接受XY卵巢移植的XX雌性并未恢复发情周期。XY卵巢的发育在形态上与XX卵巢相似，直到妊娠第16天（d.g.），此时大多数生殖细胞已到达减数分裂前期的偶线期或粗线期。然而，到分娩日（19或20 d.g.）时，XY卵巢的髓质索中已没有卵母细胞残留。在对照的XX卵巢中，第一代卵泡在髓质区域发育，并且在出生后10天，5δ-3β-羟基类固醇脱氢酶（3β-HSDH）活性首先出现在生长卵泡周围的基质细胞中。相比之下，在XY卵巢中，髓质区域未形成卵泡，3β-HSDH活性出现在无卵母细胞的髓质索的上皮细胞中。皮质区域的原始卵泡在XX和XY卵巢中均持续发育。这些结果表明，XY雌性不育是由于XY卵巢内部的缺陷所致。髓质索中卵母细胞的产前丢失可能是导致内分泌功能异常从而缺乏发情周期现象的关键事件。
