受精是一个新生命的起始。在现有受精模型中，第一个精子与卵子表面识别并结合，先后触发膜电位改变、皮质反应和透明带反应而阻止后续精子穿入（多精受精），保证受精卵（合子）基因组的二倍性。但前者是否为主因还有争议，而后两者需要30到60分钟才能发生，因此很可能还有一种快速激活的分子机制阻止后续精子穿入。我们在研究所有七种微管切割酶在小鼠卵中的定位时发现只有Fidgetin高度富集在透明带上，fidgetin敲减后进行体外受精可见受精卵多原核率显著增加。受精后五分钟检测到fidgetin形成活性六聚体，而磷酸化fidgetin在透明带上显著减少且不形成六聚体。抑制Erk活性，磷酸化 fidgetin显著减少。综上我们提出活性Fidgetin可能通过与顶体反应竞争结合关键酶Erk而作为阻止多精受精的第一道快速屏障。我们将以小鼠为模型进一步研究其作用机制，该研究将为受精的基础和应用研究做出显著贡献。

Fertilization is the beginning of a new life. In current model of mammalian fertilization, once the first sperm recognizes and binds the surface of an oocyte, change of membrane potential, cortical reaction and zona pellucida (ZP) reaction are triggered successively to prevent the entry of follow-up sperm (polyspermy), which will ensure the diploidy of the zygote (fertilized egg) genome. However, there are still arguments whether change of membrane potential is the major cause of polyspermy, and cortical reaction and ZP reaction take about 30 to 60 min to occur, so there must be a rapidly-activated molecular mechanism that can block the follow-up sperms. In our examination of the localization of all 7 microtubule severing enzymes within mouse oocytes, we found that only fidgetin highly concentrated on ZP, Fidgetin knockdown caused significantly increased polyspermy after In-vitro fertilization (IVF). Fidgetin could form active hexmer while phosphorylated fidgetin didn't at 5 min of IVF. Erk inhibition significantly decreased phosphorylated fidgetin. From above, we hypnotized that activated fidgetin might compete with acrosome reaction for the key kinase-Erk and act as the first fast barrier against polyspermy. We will use mouse as model to further investigate the mechanism and significantly contribute to the basic science and clinical application of fertilization.