Cracking the eggshell: A novel link to intracellular signaling.
Cracking the eggshell: A novel link to intracellular signaling.
复制标题
打破蛋壳：细胞内信号传导的新联系。
DOI：
10.1016/j.ydbio.2019.05.014
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发表时间：
2019
影响因子：
2.7
通讯作者：
Bembenek,JoshuaN
中科院分区：
文献类型：
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作者：
Melesse,Michael;Bembenek,JoshuaN
在有性生殖的生物体中，在减数分裂前期I停滞的卵母细胞响应激素或发育刺激而重新进入细胞周期，并在成熟过程中经历生理变化以具有受精能力。受精后，来自不同物种的卵母细胞采用保守的以及生物体特异性的调控策略，这些策略控制一系列被称为卵子激活的事件（Von Stetina和Orr-Weaver，2011）。卵子激活由精子进入触发，涉及多个并发的下游事件，包括减数分裂细胞周期的进展、细胞骨架重排、多精受精阻滞的产生以及选定的遗传性母体mRNA和蛋白质的激活和降解（Horner和Wolfner，2008）。对多精受精的阻断部分取决于细胞外基质，其在不同物种中具有不同的组成和组织。梭线虫卵母细胞是研究卵母细胞成熟和卵激活过程中复杂事件协调性的有效系统，卵激活过程中的一个关键功能是确保多精受精的阻断。受精前，减数分裂I前期停滞的卵母细胞被介导与精子相互作用的接受性卵黄层覆盖。受精后，卵黄立即通过皮质颗粒胞吐作用释放货物而被修饰，皮质颗粒胞吐作用通过添加新的蛋白质组分和酶促修饰将该接受外套转化为多精受精的阻断物（Wessel et al.，2001年）。尽管递送至卵母细胞表面的货物和由此产生的对细胞外基质的修饰在生物体之间不同，但皮质颗粒胞吐是一种高度保守的过程（Liu，2011）。In C.卵母细胞被卵黄层覆盖，卵黄层成为受精后依次建立的多层蛋壳的最外层。蛋壳由外向内包含几层：外卵黄层，几丁质层，软骨素蛋白聚糖层，称为胚外基质的区域（Gonzalez等人称为卵周间隙），渗透屏障层和胚周层（Stein和Golden，2015）。卵黄层的唯一已知标记物是含有几丁质结合结构域的蛋白CBD-1（约翰斯顿等人，2010年）。几丁质层在受精后立即在中期I通过跨膜几丁质合酶CHS-1合成（Zhang et al.，2005年）。在后期I期间发生的皮质颗粒胞吐作用释放软骨素蛋白聚糖CPG-1和CPG-2，所述软骨素蛋白聚糖CPG-1稳定地掺入软骨素蛋白聚糖层中，所述CPG-2在胚外基质内保持扩散（Bembenek等人，2007年; Olson等人，2012年）。渗透性屏障在减数分裂II期间稍后通过需要脂质生物合成的过程形成（Stein和Golden，2015; Olson等人，2012; Benenati等人，2009年）。因此，蛋壳形成和细胞周期进程紧密结合，以确保一系列高度协调的发育事件。破坏蛋壳形成的许多基因的失活也阻断极体挤出、胚胎极性的建立和其它肌动蛋白依赖性过程（约翰斯顿等人，2006年）。相比之下，剥离蛋壳的分离卵裂球在体外是可行的（埃德加和戈尔茨坦，2012），回避了为什么蛋壳突变如此严重的问题。来自González等人的新论文的结果表明，蛋壳缺陷可能会导致这些表型，这是由于蛋壳在卵母细胞向胚胎过渡期间组织信号传导的功能不受重视。
In sexually reproducing organisms, oocytes arrested in prophase I of meiosis reenter the cell cycle in response to hormonal or developmental stimulation and undergo physiological changes during maturation to become competent for fertilization. After fertilization, oocytes from different species employ conserved as well as organism-specific regulatory strategies that govern a collection of events known as egg activation (Von Stetina and Orr-Weaver, 2011). Egg activation is triggered by sperm entry and involves multiple, concurrent downstream events that include progression through the meiotic cell cycle, rearrangement of the cytoskeleton, generation of a block to polyspermy, and activation and degradation of selected inherited maternal mRNAs and proteins (Horner and Wolfner, 2008). The block to polyspermy partially depends on the extracellular matrix, which has a different composition and organization in different species. The C. elegans oocyte is a useful system for studying oocyte maturation and the coordination of the complex events during egg activation.A crucial function of the egg activation process is securing the block to polyspermy. Prior to fertilization, oocytes arrested prophase of meiosis I are covered by a receptive vitelline layer coating that mediates interactions with sperm. Immediately after fertilization, the vitelline is modified by the release of cargo through cortical granule exocytosis that converts this receptive coat into a block to polyspermy through addition of new protein components and enzymatic modifications (Wessel et al., 2001). Although the cargo delivered to the oocyte surface and the resulting modification to the extracellular matrix differs between organisms, cortical granule exocytosis is a highly conserved process (Liu, 2011). In C. elegans, the oocyte is covered by a vitelline layer that becomes the outermost layer of a multilayered eggshell built sequentially after fertilization. The eggshell contains several layers from the outside in: the outer vitelline layer, a chitin layer, the chondroitin proteoglycan layer, a region called the extra-embryonic matrix (referred to as the perivitelline space by Gonzalez et al.), the permeability barrier layer, and the peri-embryonic layer (Stein and Golden, 2015). The only known marker of the vitelline layer is the chitin-binding domain containing protein, CBD-1 (Johnston et al., 2010). The chitin layer is synthesized by the transmembrane chitin synthase, CHS-1, in metaphase I immediately after fertilization (Zhang et al., 2005). Cortical granule exocytosis, which occurs during anaphase I, releases chondroitin proteoglycans CPG-1, which is stably incorporated into the chondroitin proteoglycan layer, and CPG-2, which remains diffusive within the extra-embryonic matrix (Bembenek et al., 2007; Olson et al., 2012). The permeability barrier is made later during meiosis II by a process requiring lipid biosynthesis (Stein and Golden, 2015; Olson et al., 2012; Benenati et al., 2009). Therefore, eggshell formation and cell cycle progression are tightly integrated to ensure a highly coordinated series of developmental events. Inactivation of many genes that disrupt eggshell formation also block polar body extrusion, establishment of embryonic polarity and other actin-dependent processes (Johnston et al., 2006). In contrast, isolated blastomeres stripped of the eggshell, are viable in vitro (Edgar and Goldstein, 2012), begging the question as to why eggshell mutants are so severe. Results from the new paper from Gonzàlez et al. suggest that eggshell defects may cause these phenotypes due to an unappreciated function for the eggshell in organizing signaling during the oocyte-to-embryo transition.