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小鼠卵母细胞减数分裂恢复时间的品系差异:一种可能作用于p34cdc2激酶去磷酸化上游的细胞质因子的参与。

Strain difference in the timing of meiosis resumption in mouse oocytes: involvement of a cytoplasmic factor(s) acting presumably upstream of the dephosphorylation of p34cdc2 kinase.

作者信息

Polánski Z

机构信息

Department of Genetics and Evolution, Institute of Zoology, Jagiellonian University, Kraków, Poland.

出版信息

Zygote. 1997 May;5(2):105-9.

PMID:9276507
Abstract

Oocytes from eight inbred strains of mice were screened for the timing of germinal vesicle breakdown (GVB) in vitro. This characteristic varied between strains, reaching most extreme values in oocytes from AKR and BALB/c mice (3.1 and 1.6 h after release from dibutyryl cAMP block, respectively; p < 0.0001). The difference between AKR and BALB/c mice was confirmed in experiments in which GVB was induced in vivo by stimulation with exogenous gonadotrophins. Analysis of the rate of GVB in hybrids obtained after fusion of nuclear and cytoplasmic fragments of oocytes from both strains suggests that the factor responsible for the difference between AKR and BALB/c mice is located in the cytoplasm of the prophase oocytes. Finally, in oocytes from both strains stimulated to resume meiotic maturation with okadaic acid, an inhibitor of protein phosphatases types 1 and 2A, the rate of GVB was the same (2.2h and 2.3h for AKR and BALB/c, respectively; p=0.48). This suggests that the difference between strains is not related to the amount or quality of the pre-MPF (Maturation Promoting Factor) stored in the prophase oocyte, but to the factor(s) acting upstream of the dephosphorylation of p34cdc2 kinase in the pathway leading to pre-MPF activation.

摘要

对来自八个近交系小鼠的卵母细胞进行体外生发泡破裂(GVB)时间的筛选。该特征在不同品系间存在差异,在AKR和BALB/c小鼠的卵母细胞中达到最极端值(分别在从二丁酰环磷腺苷阻断中释放后3.1小时和1.6小时;p<0.0001)。在通过外源性促性腺激素刺激在体内诱导GVB的实验中,证实了AKR和BALB/c小鼠之间的差异。对两品系卵母细胞核质片段融合后获得的杂交种中GVB速率的分析表明,导致AKR和BALB/c小鼠之间差异的因素位于减数分裂前期卵母细胞的细胞质中。最后,在用蛋白磷酸酶1型和2A型抑制剂冈田酸刺激两品系卵母细胞恢复减数分裂成熟的实验中,GVB速率相同(AKR和BALB/c分别为2.2小时和2.3小时;p=0.48)。这表明品系间的差异与减数分裂前期卵母细胞中储存的前MPF(成熟促进因子)的量或质量无关,而是与导致前MPF激活的途径中p34cdc2激酶去磷酸化上游起作用的因子有关。

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