GPR56 is essential for testis development and male fertility in mice.
GPR56 is essential for testis development and male fertility in mice.
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DOI：
10.1002/dvdy.22468
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发表时间：
2010-12
影响因子：
2.5
通讯作者：
Xu, Lei
中科院分区：
文献类型：
--
作者：
Chen, Guangchun;Yang, Liquan;Begum, Shahinoor;Xu, Lei
睾丸的发育对于雄性的生育能力和哺乳动物物种的延续是必不可少的。睾丸的基本结构组成部分是生精小管，其内衬支持细胞，并为精子的成熟提供营养和物理保护。生精小管的形成起始于胚胎中的睾丸索，并依赖于它们在发育过程中的成熟重塑。最近，3D图像分析表明，胚胎性腺不同部位的睾丸索经历了不同的重塑过程。如何调节这种不对称重塑尚未研究。我们在这里报告，没有粘附G蛋白偶联受体，GPR 56，导致部分破坏曲细精管和降低生育力的雄性小鼠。这些缺陷似乎起源于胚胎性腺的不对称，但随后的睾丸索的初步建立，这表明GPR 56可能会采取行动，以建立一个空间和/或时间的线索，在男性性腺发育过程中的不对称索重塑。
Testis development is essential for male fertility and continuation of the mammalian species. Essential structural components of testes are seminiferous tubules, which are lined by Sertoli cells and provide nutrients and physical protection for the maturation of sperm. Seminiferous tubule formation is initiated in embryos as testis cords and relies on their remodeling for maturation during development. Recently, 3-D image analyses showed that testis cords in different parts of embryonic gonads undergo distinct remodeling processes. How this asymmetric remodeling is regulated has not been investigated. We report here that the absence of an adhesion G protein-coupled receptor, GPR56, leads to partial disruption of seminiferous tubules and reduced fertility in male mice. The defects appear to originate asymmetrically in embryonic gonads, but subsequent to the initial establishment of testis cords, suggesting that GPR56 might act to establish a spatial and/or temporal cue for asymmetric cord remodeling during male gonad development.
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