Mechanism of initiation of development via an increase of intracellular pH

卵母细胞减数分裂的重新启动通常是一个分两步进行的过程，在此过程中，第一次或第二次减数分裂的中期(中期I[MI]或中期II[MII])从前期块释放出来。虽然MI停滞在无脊椎动物中被广泛观察到，但对减数分裂中MI停滞的机制知之甚少。完全发育的海星卵母细胞在减数分裂前期的阻塞是由激素1-甲基腺嘌呤释放的。人们认为，即使没有受精，海星卵母细胞的减数分裂也是完全进行的，不会发生MI或MII停滞。在这里，我们发现海星卵母细胞的MI停滞发生在生发泡破裂后的卵巢。这种停滞是通过MOS/MEK/MAP激酶通路和阻断产卵前卵巢细胞内pH的升高来维持的。在海水中产卵后，通过与1-甲基腺嘌呤受体偶联的异三聚体G蛋白激活Na+/H+逆向转运蛋白，导致细胞内pH升高，即使在活性MAP激酶存在的情况下也能克服MI停滞。

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.