Chesnel F, Eppig J J
Jackson Laboratory, Bar Harbor, ME 04609-1500, USA.
Mol Reprod Dev. 1995 Apr;40(4):503-8. doi: 10.1002/mrd.1080400414.
This study tests the hypothesis 033 that growing murine oocytes, which are incompetent to resume meiosis, are deficient in their content of p34cdc2 and/or cyclin B, the two subunits of maturation promoting factor (MPF). Accumulation of the two MPF components occurred in an asynchronous manner in growing oocytes. Cyclin B content reached maximal levels in oocytes that were not yet competent to undergo germinal vesicle breakdown (GVB), the first obvious morphological manifestation of the resumption of meiosis. Thus, the amount of cyclin B is not the limiting factor rendering these growing oocytes incompetent to undergo GVB. In contrast, synthesis and accumulation of p34cdc2 increased during the period of oocyte growth in vivo when they became competent to undergo GVB. A similar increase in the amount of p34cdc2 also occurred in cultured granulosa cell-free oocytes despite the lack of oocyte growth, but these cultured oocytes did not become GVB competent. Thus, the accumulation of p34cdc2 is probably necessary, but not sufficient, for mouse oocytes to become competent to undergo GVB. This accumulation occurs autonomously in oocytes independently of growth or of the participation of follicular somatic cells.
本研究检验了假说033：生长中的小鼠卵母细胞无法恢复减数分裂，其成熟促进因子（MPF）的两个亚基p34cdc2和/或细胞周期蛋白B的含量不足。在生长中的卵母细胞中，这两种MPF成分以异步方式积累。细胞周期蛋白B的含量在尚未具备生发泡破裂（GVB）能力的卵母细胞中达到最高水平，GVB是减数分裂恢复的首个明显形态学表现。因此，细胞周期蛋白B的量不是使这些生长中的卵母细胞无法进行GVB的限制因素。相比之下，在体内卵母细胞生长至具备GVB能力的期间，p34cdc2的合成与积累增加。尽管缺乏卵母细胞生长，但在培养的无颗粒细胞卵母细胞中p34cdc2的量也有类似增加，不过这些培养的卵母细胞并未获得GVB能力。因此，p34cdc2的积累可能是小鼠卵母细胞具备GVB能力所必需的，但并不充分。这种积累在卵母细胞中自主发生，与生长或卵泡体细胞的参与无关。
