Picard A, Dorée M
Exp Cell Res. 1983 May;145(2):325-37. doi: 10.1016/0014-4827(83)90011-3.
Microinjection of EGTA into prophase-blocked oocytes does not inhibit hormone-induced meiosis reinitiation, although it prevents oocyte activation by fertilization, by ionophore A23187, or by subsequent microinjection of otherwise efficient Ca2+ buffers. In contrast microinjection of Ca2+ buffers inhibits 1-methyladenine-induced meiosis reinitiation. Oocytes can be released from Ca2+ inhibition by raising hormone concentration or by the subsequent transfer of cytoplasm taken from maturing oocytes. Ca2+-microinjected oocytes remain inhibited up to 1 h after microinjection, although free Ca2+ concentration comes back to its resting value less than 30 sec after microinjection. Cyanide, which decreases ATP content and depresses Ca2+-pumping activity, reversibly inhibits 1-methyladenine-induced meiosis reinitiation. These results do not support the hypothesis that Ca2+ is the second messenger of the hormone in meiosis reinitiation of starfish oocytes, although they support the view that elimination of Ca2+ from some component of the oocyte cortex (perhaps the plasma membrane) might be a compulsory event for transduction of the hormonal message.
向处于前期阻滞的卵母细胞中微量注射乙二醇双（2-氨基乙醚）四乙酸（EGTA），虽可阻止受精、离子载体A23187或后续微量注射其他有效的钙离子缓冲液诱导的卵母细胞激活，但不会抑制激素诱导的减数分裂重新启动。相比之下，微量注射钙离子缓冲液会抑制1-甲基腺嘌呤诱导的减数分裂重新启动。提高激素浓度或随后转移取自成熟卵母细胞的细胞质，可使卵母细胞从钙离子抑制状态中释放出来。微量注射钙离子的卵母细胞在注射后长达1小时仍处于抑制状态，尽管微量注射后不到30秒，游离钙离子浓度就会恢复到静息值。氰化物会降低三磷酸腺苷（ATP）含量并抑制钙离子泵活性，它能可逆地抑制1-甲基腺嘌呤诱导的减数分裂重新启动。这些结果并不支持钙离子是激素在海星卵母细胞减数分裂重新启动过程中的第二信使这一假说，尽管它们支持这样一种观点，即从卵母细胞皮层的某些成分（可能是质膜）中去除钙离子，可能是激素信号转导的一个必要事件。
