In the present work, we described the expression and activity of extracellular signal-related kinases 1-2 (ERK1-2) in mouse primordial germ cells (PGCs) from 8.5–14.5 days post coitum (dpc) and investigated whether these kinases play a role in regulating the various processes of PGC development. Using immunofluorescence and immunoblotting to detect the active phosphorylated form of ERK1-2 (p-ERK1-2), we found that the kinases were present in most proliferating 8.5–10.5 dpc PGCs, low in 11.5 dpc PGCs, and progressively increasing between 12.5–14.5 dpc both in female and male PGCs. In vitro culture experiments showed that inhibiting activation of ERK1-2 with the MEK-specific inhibitor U0126 significantly reduced the growth of 8.5 dpc PGCs in culture but had little effect on 11.5–12.5 dpc PGCs. Moreover, we found that the inhibitor did not affect the adhesion of 11.5 dpc PGCs, but it significantly reduced their motility features onto a cell monolayer. Further, while the ability of female PGCs to begin meiosis was not significantly affected by U0126, their progression through meiotic prophase I was slowed down. Notably, the activity of ERK1-2 was necessary for maintaining the correct expression of oocyte-specific genes crucial for germ cells survival and the formation of primordial follicles.

中文翻译：

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细胞外信号相关激酶 1-2 (ERK1-2) 在小鼠原始生殖细胞发育中的表达和可能的作用

在目前的工作中，我们描述了性交后 8.5-14.5 天 (dpc) 小鼠原始生殖细胞 (PGC) 中细胞外信号相关激酶 1-2 (ERK1-2) 的表达和活性，并研究了这些激酶是否发挥在调节 PGC 发育的各种过程中的作用。使用免疫荧光和免疫印迹检测 ERK1-2 (p-ERK1-2) 的活性磷酸化形式，我们发现激酶存在于大多数增殖的 8.5-10.5 dpc PGC 中，11.5 dpc PGC 中的低，并在 12.5- 之间逐渐增加在女性和男性 PGC 中均为 14.5 dpc。体外培养实验表明，用 MEK 特异性抑制剂 U0126 抑制 ERK1-2 的激活显着降低了培养中 8.5 dpc PGC 的生长，但对 11.5-12.5 dpc PGC 几乎没有影响。此外，我们发现抑制剂不影响 11.5 dpc PGC 的粘附，但它显着降低了它们在细胞单层上的运动特征。此外，虽然雌性 PGC 开始减数分裂的能力不受 U0126 的显着影响，但它们通过减数分裂前期 I 的进程减慢了。值得注意的是，ERK1-2 的活性对于维持对生殖细胞存活和原始卵泡形成至关重要的卵母细胞特异性基因的正确表达是必要的。