Moses R M, Kline D
Department of Zoology, University of Toronto, Canada.
Mol Reprod Dev. 1995 Jun;41(2):264-73. doi: 10.1002/mrd.1080410218.
Mouse egg activation, which includes release from meiotic metaphase II arrest, results from fertilization-induced increase in intracellular calcium concentration ([Ca2+]i). However, during egg activation caused by exposure to the protein synthesis inhibitor, cycloheximide, [Ca2+]i did not change. Although eggs fertilized in the presence of microtubule inhibitors remain arrested at metaphase, eggs treated for 32 hr with cycloheximide and the microtubule inhibitor, colcemid, formed nuclei. In untreated eggs aged in culture for 24 hr, the microtubule spindles became deformed. These eggs formed nuclei after exposure to cycloheximide, but not the calcium ionophore A23187. Our results indicate that eggs in which protein synthesis is inhibited are released from metaphase without an increase in [Ca2+]i, and despite disruption of the spindle.
小鼠卵母细胞激活包括从减数第二次分裂中期阻滞中释放出来,这是由受精诱导的细胞内钙浓度([Ca2+]i)升高所导致的。然而,在由蛋白质合成抑制剂环己酰亚胺引起的卵母细胞激活过程中,[Ca2+]i并未改变。尽管在微管抑制剂存在的情况下受精的卵母细胞仍停滞在中期,但用环己酰亚胺和微管抑制剂秋水仙酰胺处理32小时的卵母细胞形成了细胞核。在体外培养24小时的未处理老化卵母细胞中,微管纺锤体发生变形。这些卵母细胞在暴露于环己酰亚胺后形成了细胞核,但暴露于钙离子载体A23187后则未形成。我们的结果表明,蛋白质合成受到抑制的卵母细胞在[Ca2+]i没有升高的情况下从中期释放出来,并且尽管纺锤体受到破坏。