Lambert Charles C
University of Washington Friday Harbor Laboratories, 620 University Road, Friday Harbor, WA 98250, USA.
Dev Growth Differ. 2008 Mar;50(3):181-8. doi: 10.1111/j.1440-169X.2008.00983.x. Epub 2008 Feb 27.
Many ascidian oocytes undergo 'spontaneous' germinal vesicle breakdown (GVBD) when transferred from the ovary to normal pH 8.2 sea water (SW); however, low pH inhibits GVBD, which can then be stimulated while remaining in the low pH SW. Oocytes of Boltenia villosa blocked from GVBD by pH 4 SW undergo GVBD in response to permeant cyclic AMP (8-bromo-cyclic AMP), phosphodiesterase inhibitors (isobutylmethylxanthine and theophylline) or the adenylyl cyclase activator forskolin. This suggests that cAMP increases during GVBD. Removal of the follicle cells or addition of a protease inhibitor inhibits GVBD in response to raised pH but not to forskolin, theophylline or 8 bromo-cAMP. Isolated follicle cells in low pH SW release protease activity in response to an increase in pH. These studies imply that the follicle cells release protease activity, which either itself stimulates an increase in oocyte cAMP level or reacts with other molecules to stimulate this process. Studies with the mitogen-activated protein (MAP) kinase inhibitors U0126 and CI 1040 suggest that MAP kinase is not involved in GVBD. The Cdc25 inhibitor NSC 95397 inhibits GVBD at 200 nm in a reversible manner.
许多海鞘卵母细胞从卵巢转移至正常pH 8.2的海水（SW）中时会发生“自发”的生发泡破裂（GVBD）；然而，低pH会抑制GVBD，随后在低pH的SW中可刺激其发生GVBD。被pH 4的SW阻断GVBD的绒毛博尔特海鞘卵母细胞会对渗透性环磷酸腺苷（8-溴环磷酸腺苷）、磷酸二酯酶抑制剂（异丁基甲基黄嘌呤和茶碱）或腺苷酸环化酶激活剂福斯高林产生反应而发生GVBD。这表明在GVBD过程中环磷酸腺苷（cAMP）会增加。去除卵泡细胞或添加蛋白酶抑制剂会抑制因pH升高引起的GVBD，但不会抑制对福斯高林、茶碱或8-溴环磷酸腺苷的反应。低pH的SW中的分离卵泡细胞会因pH升高而释放蛋白酶活性。这些研究表明，卵泡细胞释放蛋白酶活性，其本身要么刺激卵母细胞cAMP水平升高，要么与其他分子反应以刺激这一过程。用丝裂原活化蛋白（MAP）激酶抑制剂U0126和CI 1040进行的研究表明，MAP激酶不参与GVBD。Cdc25抑制剂NSC 95397在200 nM时以可逆方式抑制GVBD。
