Wortzman-Show Genevieve B, Kurokawa Manabu, Fissore Rafael A, Evans Janice P
Division of Reproductive Biology, Department of Biochemistry and Molecular Biology, Johns Hopkins University, Bloomberg School of Public Health, Room W3606, 615 North Wolfe Street, Baltimore, MD 21205, USA.
Mol Hum Reprod. 2007 Aug;13(8):557-65. doi: 10.1093/molehr/gam042. Epub 2007 Jun 16.
One important result of egg activation is the establishment of blocks to prevent polyspermic fertilization; these blocks are established on the zona pellucida and the egg plasma membrane. This study examines what the sperm brings to the egg to induce the establishment of the membrane block to polyspermy, building on past evidence that membrane block establishment does not occur in response to parthenogenetic stimuli that induce a single transient increase in cytosolic Ca2+ or intracytoplasmic sperm injection (ICSI). We test the hypotheses that (i) sperm-associated Ca2+ release activity triggers membrane block establishment; (ii) introduction of sperm contents via variations on ICSI protocols (resulting in improved Ca2+ transients, egg activation and embryo development over traditional ICSI protocols) triggers membrane block establishment and (iii) sperm adhesion [binding of an extracellular sperm ligand(s) to an egg receptor(s)] combined with sperm-associated Ca2+ release activity triggers membrane block establishment. Interestingly, none of these stimuli induced establishment of the membrane block to polyspermy in mouse eggs. However, the sperm-associated remodeling of the egg cortical cytoskeleton differs between conventionally fertilized and ICSI-fertilized eggs; taken with our previous data implicating actin microfilaments in membrane block establishment, this raises the possibility that cortical reorganization may be a contributing factor. In sum, fertilization-like Ca2+ transients, either alone or combined with sperm-egg binding, are not sufficient for membrane block establishment, but that an event(s) associated with gamete interaction plays a role in this membrane function change.
卵子激活的一个重要结果是建立防止多精受精的屏障；这些屏障建立在透明带和卵质膜上。本研究基于以往的证据，即膜屏障的建立不会发生在诱导胞质Ca2+单次短暂增加的孤雌生殖刺激或胞质内精子注射（ICSI）之后，探讨精子带给卵子的物质是什么，从而诱导建立对多精受精的膜屏障。我们检验了以下假设：（i）精子相关的Ca2+释放活性触发膜屏障的建立；（ii）通过对ICSI方案的改进（与传统ICSI方案相比，能产生更好的Ca2+瞬变、卵子激活和胚胎发育）引入精子内容物触发膜屏障的建立；（iii）精子黏附（细胞外精子配体与卵子受体结合）与精子相关的Ca2+释放活性共同触发膜屏障的建立。有趣的是，这些刺激均未在小鼠卵子中诱导建立对多精受精的膜屏障。然而，常规受精和ICSI受精的卵子中，精子相关的卵子皮质细胞骨架重塑存在差异；结合我们之前关于肌动蛋白微丝参与膜屏障建立的数据，这增加了皮质重组可能是一个促成因素的可能性。总之，类似受精的Ca2+瞬变，单独或与精卵结合相结合，不足以建立膜屏障，但与配子相互作用相关的一个或多个事件在这种膜功能变化中起作用。
