Potency of testicular somatic environment to support spermatogenesis in XX/Sry transgenic male mice
Potency of testicular somatic environment to support spermatogenesis in XX/Sry transgenic male mice
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DOI：
10.1242/dev.02751
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发表时间：
2007-02-01
期刊：
影响因子：
4.6
通讯作者：
Kanai, Yoshiakira
中科院分区：
文献类型：
--
作者：
Ishii, Mayuko;Tachiwana, Tsuyoshi;Kanai, Yoshiakira
Chr Y（Sry）基因的性别决定区足以诱导染色体雌性小鼠和人类的睾丸形成和随后的内生殖器和外生殖器的雄性发育。然而，在XX性别逆转的雄性中，例如XX/Sry转基因（XX/Sry）小鼠，由于生殖细胞自主缺陷，睾丸生殖细胞总是在出生后不久消失。因此，尚不清楚单独的Sry是否足以诱导能够支持XX体内完整精子发生的功能齐全的睾丸索马。在这里，我们证明了XX/Sry男性的睾丸体细胞环境是有缺陷的，在支持精子发生的后期阶段。使用XX/Sry雄性小鼠的精原细胞移植分析显示，供体XY精原细胞能够增殖，进入减数分裂并分化为圆形精子细胞阶段。然而，XY供体衍生的圆形精子细胞经常从XX/Sry生精上皮细胞上脱落并发生细胞死亡，导致精子细胞阶段严重缺乏。相比之下，未成熟的XY曲细精管段XX/Sry睾丸包膜下移植清楚地显示出适当的分化成细长的精子细胞在移植的XY供体小管。从XX/Sry睾丸中分离的曲细精管的微阵列分析证实了几个Y-连锁基因的缺失表达和与精子发生相关的基因表达谱的改变。因此，我们的研究结果表明XX/Sry睾丸的体细胞小管成分（可能是支持细胞）功能障碍，突出了Sry单独不足以在XX小鼠中诱导功能齐全的支持细胞的想法。
The sex-determining region of Chr Y (Sry) gene is sufficient to induce testis formation and the subsequent male development of internal and external genitalia in chromosomally female mice and humans. In XX sex-reversed males, such as XX/Sry-transgenic (XX/Sry) mice, however, testicular germ cells always disappear soon after birth because of germ cell-autonomous defects. Therefore, it remains unclear whether or not Sry alone is sufficient to induce a fully functional testicular soma capable of supporting complete spermatogenesis in the XX body. Here, we demonstrate that the testicular somatic environment of XX/Sry males is defective in supporting the later phases of spermatogenesis. Spermatogonial transplantation analyses using XX/Sry male mice revealed that donor XY spermatogonia are capable of proliferating, of entering meiosis and of differentiating to the round-spermatid stage. XY-donor-derived round spermatids, however, were frequently detached from the XX/Sry seminiferous epithelia and underwent cell death, resulting in severe deficiency of elongated spermatid stages. By contrast, immature XY seminiferous tubule segments transplanted under XX/Sry testis capsules clearly displayed proper differentiation into elongated spermatids in the transplanted XY-donor tubules. Microarray analysis of seminiferous tubules isolated from XX/Sry testes confirmed the missing expression of several Y-linked genes and the alterations in the expression profile of genes associated with spermiogenesis. Therefore, our findings indicate dysfunction of the somatic tubule components, probably Sertoli cells, of XX/Sry testes, highlighting the idea that Sry alone is insufficient to induce a fully functional Sertoli cell in XX mice.