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钙刺激后新成熟或微管耗尽的小鼠卵母细胞中的中期阻滞。

Metaphase arrest in newly matured or microtubule-depleted mouse eggs after calcium stimulation.

作者信息

Moses R M, Masui Y

机构信息

Department of Zoology, University of Toronto, Canada.

出版信息

Zygote. 1995 Feb;3(1):1-8. doi: 10.1017/s0967199400002318.

Abstract

In mouse eggs arrested at meiotic metaphase II, the increase in intracellular calcium that results from fertilisation induces nuclear formation in both newly ovulated and older eggs. In contrast, the calcium increase that results from exposure to the calcium ionophore A23187 induces nuclear formation in older, but not young, newly ovulated eggs. When treated with the microtubule inhibitor colcemid, and fertilised, young eggs remained at metaphase, but many older eggs formed nuclei, although older eggs treated with colcemid and A23187 remained at metaphase. However, young A23187-treated eggs, young colcemid-treated fertilised eggs, and older colcemid- and A23187-treated eggs, formed nuclei when treated, in addition, with the protein synthesis inhibitor cycloheximide, or the protein kinase inhibitor 6-dimethylaminopurine (6-DMAP). The possibility is discussed that metaphase in newly matured eggs and microtubule-depleted eggs may be maintained by similar mechanisms involving short-lived phosphorylated proteins.

摘要

在减数分裂中期II停滞的小鼠卵中,受精导致的细胞内钙增加会诱导新排卵的卵和较老的卵形成细胞核。相比之下,暴露于钙离子载体A23187导致的钙增加会诱导较老的新排卵卵形成细胞核,但不会诱导年轻的新排卵卵形成细胞核。用微管抑制剂秋水仙酰胺处理并受精后,年轻的卵停留在中期,但许多较老的卵形成了细胞核,尽管用秋水仙酰胺和A23187处理的较老的卵仍停留在中期。然而,用蛋白质合成抑制剂环己酰亚胺或蛋白激酶抑制剂6-二甲基氨基嘌呤(6-DMAP)处理后,经A23187处理的年轻卵、经秋水仙酰胺处理的受精年轻卵以及经秋水仙酰胺和A23187处理的较老的卵都会形成细胞核。文中讨论了新成熟的卵和微管缺失的卵中的中期可能通过涉及短寿命磷酸化蛋白的类似机制得以维持的可能性。

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