蛋白激酶在卵母细胞减数分裂和受精中的作用

脊椎动物卵母细胞的减数分裂和受精过程受到多种蛋白激酶的调节。近年来对于卵母细胞成熟、活化和受精的分子机制研究取得了长足进步 ,发现促成熟因子 (MPF)和促分裂原活化蛋白激酶 (MAPK)是调节卵母细胞细胞周期的关键分子 ,二者的激活和失活导致了减数分裂的恢复、阻滞和完成。许多蛋白激酶通过调节MPF和MAPK活性来影响减数分裂。Polo like激酶活化MPF ,Mos激活MAPK而启动成熟分裂并维持中期阻滞。CaMKII通过泛素途径灭活MPF使卵突破MII期阻滞。另外 ,p90 rsk作为MAPK的下游分子参与减数分裂调节 ,蛋白激酶C(PKC)诱导皮质颗粒排放并抑制MAPK激活 ,酪氨酸蛋白激酶家族成员介导受精诱发的Ca2 释放。这些蛋白激酶的协同作用推动了卵母细胞正常的成熟与受精

Protein Kinases Involved in the Meiotic Maturation and Fertilization of Oocyte

The meiosis and fertilization of vertebrate oocyte are extensively regulated by various protein kina- ses. Recently, a great progress has been achieved in the studies on the molecular mechanisms of oocyte maturation, activation and fertilization. MPF and MAPK were found to be the key modulators of the cell cycle in oocyte, whose activation and inactivation result in the entry, arrest and exit of meiosis. Many protein kinases influence the meiosis by stimulating or inhibiting the activity of MPF and MAPK. Polo-like kinase activates MPF, whereas Mos initiates oocyte maturation and sustains MII arrest by activating MAPK. CaMK II down-regulates the MPF level through an ubiquitin-dependent pathway, which leads to the breakthrough of M phase arrest. Furthermore, p90 rsk is involved in the meiosis regulation as a downstream regulator of MAPK; protein kinase C induces cortical granule exocytosis after fertilization and inhibits MAPK activity during maturation; and tyrosine protein kinase family members modulate the calcium release induced by fertilization. The cooperation of these protein kinases is essential to the development and fertilization of the oocyte.