Anifandis George, Messini Christina I, Dafopoulos Konstantinos, Daponte Alexandros, Messinis Ioannis E
Department of Obstetrics and Gynaecology, ART Unit, University of Thessaly, School of Health Sciences, Faculty of Medicine, Larissa, Greece.
J Assist Reprod Genet. 2016 Mar;33(3):313-316. doi: 10.1007/s10815-016-0653-0. Epub 2016 Jan 16.
It is well known that for successful fertilization, oocyte activation is required, which involves a signal transduction cascade leading to the conversion of the oocyte to a diploid embryo. During oocyte activation, intracellular calcium levels oscillate repetitively causing exocytosis of cortical granules, the enzymes which the latter contain are released into the perivitelline space, leading to modifications of the zona pellucida (ZP), which prevent the penetration of the ZP by further spermatozoa. The necessary element that initiates oocyte activation is apparently the release of intracellular calcium (Ca(2+)) stored in the endoplasmic reticulum (ER). The exact mechanism via which Ca(2+) is released within the oocyte has not been yet clarified, and has been a matter of an ongoing debate. Today, the sperm factor hypothesis has gained general acceptance, according to which a sperm molecule, either phospholipase C (PLCζ) or a post-acrosomal sheath WW domain-binding protein (PAWP), diffuses into the ooplasm initiating a molecular cascade involving mainly the phosphoinositide pathway. Mounting evidence now indicates that these calcium oscillations are caused by a testis-specific PLC termed PLCζ, released into the oocyte following gamete fusion. Also, recently, PAWP has been proposed as an alternative sperm factor candidate. These different sperm candidates have led to a significant debate. This raises important questions as regards to the relative importance of these two proteins as diagnostic tools in reproductive medicine with therapeutic potential, indicating the need for further research. In the present mini review, the phenomenon of oocyte activation during fertilization as well as the existing controversy will be highlighted and the possible mechanisms that are involved in this process will be discussed. Finally, an explanation of the existing debate will be attempted.
众所周知，成功受精需要卵母细胞激活，这涉及一个信号转导级联反应，导致卵母细胞转变为二倍体胚胎。在卵母细胞激活过程中，细胞内钙水平反复振荡，引起皮质颗粒的胞吐作用，皮质颗粒所含的酶被释放到卵周隙中，导致透明带（ZP）发生修饰，从而阻止更多精子穿透透明带。启动卵母细胞激活的必要因素显然是内质网（ER）中储存的细胞内钙（Ca(2+)）的释放。Ca(2+)在卵母细胞内释放的确切机制尚未阐明，一直是一个持续争论的问题。如今，精子因子假说已被广泛接受，根据该假说，一种精子分子，即磷脂酶C（PLCζ）或顶体后鞘WW结构域结合蛋白（PAWP），扩散到卵质中，引发一个主要涉及磷脂酰肌醇途径的分子级联反应。现在越来越多的证据表明，这些钙振荡是由一种睾丸特异性的PLC，即PLCζ引起的，它在配子融合后释放到卵母细胞中。此外，最近PAWP也被提议作为另一种精子因子候选物。这些不同的精子候选物引发了激烈的争论。这就生殖医学中这两种蛋白作为具有治疗潜力的诊断工具的相对重要性提出了重要问题，表明需要进一步研究。在本综述中，将重点介绍受精过程中卵母细胞激活的现象以及现有的争议，并讨论该过程中可能涉及的机制。最后，将尝试对现有争论进行解释。
