Zhang Lian-Jun, Chen Bo, Feng Xin-Lei, Ma Hua-Gang, Sun Li-Lan, Feng Yan-Min, Liang Gui-Jin, Cheng Shun-Feng, Li Lan, Shen Wei
Key Laboratory of Animal Reproduction and Germplasm Enhancement in Universities of Shandong, Qingdao Agricultural University, Qingdao, 266109, China.
Center for Reproductive Biology, Weifang People's Hospital, Weifang, 261041, China.
Reprod Fertil Dev. 2015 Jan;27(2):294-303. doi: 10.1071/RD13281.
In mammals, ontogenesis starts from a fusion of spermatozoon and oocyte, which are produced by reductive nuclear division of a diploid germ cell in a specialised but complex biological process known as meiosis. However, little is known about the mechanism of meiotic initiation in germ cells, although many factors may be responsible for meiosis both in male and female gonads. In this study, 11.5 days post coitum (dpc) female fetal mouse genital ridges were cultured in vitro with exposure to Brefeldin A (BFA) for 6h, and the changes in meiosis were detected. Synaptonemal-complex analysis implied that BFA played a positive role in meiosis initiation and this hypothesis was confirmed by quantitative PCR of meiosis-specific genes: stimulated by retinoic acid gene 8 (Stra8) and deleted in a zoospermia-like (DAZL). At the same time, mRNA expression of retinoic acid synthetase (Raldh2) and retinoic acid (RA) receptors increased in female gonads with in vitro exposure to BFA. Transplanting genital ridges treated with BFA into the kidney capsule of immunodeficient mice demonstrated that the development capacity of female germ cells was normal, while formation of primordial follicles was seen to be a result of accelerated meiosis after exposure to BFA. In conclusion, the study indicated that BFA stimulated meiosis initiation partly by RA signalling and then promoted the development of follicles.
在哺乳动物中，个体发育始于精子与卵子的融合，精子和卵子是由二倍体生殖细胞通过一种特殊但复杂的生物过程（即减数分裂）进行的减数核分裂产生的。然而，尽管许多因素可能在雄性和雌性性腺中对减数分裂起作用，但关于生殖细胞减数分裂起始的机制却知之甚少。在本研究中，将交配后11.5天（dpc）的雌性胎鼠生殖嵴进行体外培养，使其暴露于布雷菲德菌素A（BFA）6小时，并检测减数分裂的变化。联会复合体分析表明，BFA在减数分裂起始中起积极作用，这一假设通过减数分裂特异性基因的定量PCR得到证实：受视黄酸刺激基因8（Stra8）和无精症样缺失基因（DAZL）。同时，体外暴露于BFA的雌性性腺中视黄酸合成酶（Raldh2）和视黄酸（RA）受体的mRNA表达增加。将经BFA处理的生殖嵴移植到免疫缺陷小鼠的肾囊中表明，雌性生殖细胞的发育能力正常，而原始卵泡的形成被认为是暴露于BFA后减数分裂加速的结果。总之，该研究表明，BFA部分通过RA信号刺激减数分裂起始，进而促进卵泡发育。
