Unfertilized eggs of most animals are arrested at a certain point in the meiotic cell cycles. Reinitiation of meiosis and the start of embryogenesis are triggered by fertilization. This arrest is essential for preventing parthenogenetic activation and for promoting proper initiation of development by fertilization. In the larvacean Oikopleura dioica, which is a simple model organism for studies of chordate development, the unfertilized egg is arrested at metaphase of meiosis I. We show here that protein phosphatase 2A (PP2A) is essential for maintenance of meiotic arrest after spawning of oocytes. Knockdown (KD) of the maternal PP2A catalytic subunit, which was found in functional screening of maternal factors, caused unfertilized eggs to spontaneously release polar bodies after spawning, and then start pseudo-cleavages without fertilization, namely, parthenogenesis. Parthenogenetic embryos failed to undergo proper mitosis and cytokinesis because of lack of a centrosome, which is to be brought into the egg by a sperm. Activation of the KD oocytes was triggered by possible rise of ambient and intracellular pH upon their release from the gonad into seawater at spawning. Live recording of intracellular calcium level of the KD oocytes indicated that the pH rise caused an aberrant Ca²⁺ burst, which mimicked the Ca²⁺ burst that occurs at fertilization. Then, the aberrant Ca²⁺ burst triggered meiosis resumption through Calcium/calmodulin-dependent protein kinase (CaMK II). Therefore, PP2A is essential for maintenance of meiotic arrest and prevention of parthenogenesis by suppressing the aberrant Ca²⁺ burst at spawning.

大多数动物的未受精卵会在减数分裂细胞周期的某个时刻停滞。受精触发减数分裂的重新开始和胚胎发生的开始。该阻止对于防止孤雌生殖激活和通过受精促进发育的适当启动至关重要。在幼虫Oikopleura dioica，这是一种用于研究卵酸盐发育的简单模型生物，未受精的卵被阻滞在减数分裂I的中期。我们在此处显示，卵母细胞产卵后蛋白磷酸酶2A（PP2A）对于维持减数分裂阻滞至关重要。在母体因子的功能筛选中发现的母体PP2A催化亚基的敲低（KD）导致未受精卵产卵后自发释放极体，然后在不受精的情况下开始假卵裂，即孤雌生殖。单性生殖胚胎由于缺乏中心体而无法进行适当的有丝分裂和胞质分裂，中心体要由精子带入卵中。KD卵母细胞的激活是由产卵时从性腺释放到海水中时环境和细胞内pH可能升高引起的。²⁺爆发，模仿受精时发生的Ca ²⁺爆发。然后，异常的Ca ²⁺爆发通过钙/钙调蛋白依赖性蛋白激酶（CaMK II）触发减数分裂恢复。因此，PP2A通过抑制产卵时异常的Ca ²⁺爆发对于维持减数分裂停滞和防止孤雌生殖至关重要。