Hashimoto N, Kishimoto T
Department of Developmental Biology, National Institute for Basic Biology, Okazaki, Japan.
Dev Biol. 1988 Apr;126(2):242-52. doi: 10.1016/0012-1606(88)90135-2.
During mouse oocyte maturation the regulation of the activity of a cytoplasmic maturation-promoting factor (MPF) was examined. The mouse MPF activity was determined based on its ability to induce maturation in immature starfish oocytes after microinjection with the cytoplasm from mouse oocytes. MPF appeared initially at germinal vesicle breakdown (GVBD), and its activity fluctuated in exact correspondence with meiotic cycles, reaching a peak at each metaphase and almost disappearing at the time of emission of the first polar body. Cycloheximide affected neither the initial MPF appearance nor GVBD. Thereafter, however, in the presence of cycloheximide the meiotic spindle was not formed and MPF disappeared, although the chromosomes remained condensed. After removing cycloheximide, MPF reappeared and was followed by the first metaphase and subsequently by polar body emission. Finally the meiotic cycle progressed to the second metaphase. Thus, for the appearance of MPF, there is a critical period shortly before the first metaphase, after which protein synthesis is required. In the presence of either cytochalasin D or colcemid, MPF activity remained at elevated levels. Addition of cycloheximide to such cytochalasin-treated oocytes, in which the meiotic cycle was arrested at the first metaphase, caused the MPF levels to decrease and was followed by movement of chromosomes to both poles where they decondensed and two nucleus-like structures were formed. Thus, the disappearance of MPF may initiate the metaphase-anaphase transition. Furthermore, detailed cytological examination revealed that chromosomes in cytochalasin-treated oocytes were monovalent while those treated only with cycloheximide were divalent, suggesting that dissociation of the synapsis is a prerequisite for chromosome decondensation after the disappearance of MPF. In all these respects, MPF seems to be a metaphase-promoting factor rather than just a maturation-promoting factor.
在小鼠卵母细胞成熟过程中，对细胞质成熟促进因子（MPF）活性的调节进行了研究。小鼠MPF活性是根据其在显微注射小鼠卵母细胞的细胞质后诱导未成熟海星卵母细胞成熟的能力来确定的。MPF最初出现在生发泡破裂（GVBD）时，其活性与减数分裂周期精确波动，在每个中期达到峰值，并在第一极体排出时几乎消失。放线菌酮既不影响MPF的最初出现，也不影响GVBD。然而，此后，在放线菌酮存在的情况下，减数分裂纺锤体未形成，MPF消失，尽管染色体仍保持浓缩状态。去除放线菌酮后，MPF重新出现，随后是第一次中期，接着是极体排出。最后，减数分裂周期进展到第二次中期。因此，对于MPF的出现，在第一次中期前不久有一个关键时期，在此之后需要蛋白质合成。在细胞松弛素D或秋水仙酰胺存在的情况下，MPF活性保持在较高水平。向这种细胞松弛素处理的卵母细胞（减数分裂周期停滞在第一次中期）中添加放线菌酮，会导致MPF水平下降，随后染色体向两极移动，在那里它们解聚并形成两个核样结构。因此，MPF的消失可能启动中期 - 后期转换。此外，详细细胞学检查显示，细胞松弛素处理的卵母细胞中的染色体是单价的，而仅用放线菌酮处理的卵母细胞中的染色体是二价的，这表明联会的解离是MPF消失后染色体解聚的先决条件。在所有这些方面，MPF似乎是一个中期促进因子，而不仅仅是一个成熟促进因子。
