Harada Kaori, Oita Eiko, Chiba Kazuyoshi
Department of Biology, Ochanomizu University, 2-1-1 Ohtsuka, Bunkyo-ku, Tokyo 112-8610, Japan.
Development. 2003 Oct;130(19):4581-6. doi: 10.1242/dev.00649.
Reinitiation of meiosis in oocytes usually occurs as a two-step process during which release from the prophase block is followed by an arrest in metaphase of the first or second meiotic division [metaphase I (MI) or metaphase II (MII)]. The mechanism of MI arrest in meiosis is poorly understood, although it is a widely observed phenomenon in invertebrates. The blockage of fully grown starfish oocytes in prophase of meiosis I is released by the hormone 1-methyladenine. It has been believed that meiosis of starfish oocytes proceeds completely without MI or MII arrest, even when fertilization does not occur. Here we show that MI arrest of starfish oocytes occurs in the ovary after germinal vesicle breakdown. This arrest is maintained both by the Mos/MEK/MAP kinase pathway and the blockage of an increase of intracellular pH in the ovary before spawning. Immediately after spawning into seawater, activation of Na+/H+ antiporters via a heterotrimeric G protein coupling to a 1-methyladenine receptor in the oocyte leads to an intracellular pH increase that can overcome the MI arrest even in the presence of active MAP kinase.
卵母细胞减数分裂的重新启动通常是一个两步过程，在此过程中，从前期阻滞释放后会在第一次或第二次减数分裂的中期（中期I或中期II）发生停滞。减数分裂中期I停滞的机制尚不清楚，尽管这是在无脊椎动物中广泛观察到的现象。完全成熟的海星卵母细胞在减数分裂I前期的阻滞通过激素1-甲基腺嘌呤解除。人们一直认为，即使未发生受精，海星卵母细胞的减数分裂也能完全进行，不会出现中期I或中期II停滞。在此我们表明，海星卵母细胞的中期I停滞发生在生发泡破裂后的卵巢中。这种停滞通过Mos/MEK/MAP激酶途径以及产卵前卵巢中细胞内pH升高的阻滞得以维持。刚产入海水中后，通过异源三聚体G蛋白与卵母细胞中的1-甲基腺嘌呤受体偶联而激活Na+/H+反向转运体，导致细胞内pH升高，即使在存在活性MAP激酶的情况下也能克服中期I停滞。
