Stazione Zoologica Anton Dohrn, Napoli, Italy.
Acta Physiol (Oxf). 2009 Jan;195(1):61-70. doi: 10.1111/j.1748-1716.2008.01921.x.
Starfish oocytes undergo massive intracellular Ca2+ signalling during meiotic maturation and fertilization. Although the igniting stimulus of Ca2+ mobilization may differ in different cell contexts, its final leverage is usually the Ca2+-releasing second messengers such as InsP3, cADPr and NAADP. The general scheme of intracellular Ca2+ release is that the corresponding receptors for these molecules serve as ion channels to release free Ca2+ from its internal stores such as the lumen of the endoplasmic reticulum. However, a growing body of evidence has suggested that intracellular Ca2+ release can be strongly modulated by the actin cytoskeleton. Although it is known that Ca2+ contributes to remodelling of the actin cytoskeleton, whether the actin cytoskeleton modulates Ca2+ signalling in return has not been much explored. An emerging candidate to answer to this reciprocal causality of Ca2+ and the actin cytoskeleton may be actin-binding proteins. In this review, we discuss how the actin cytoskeleton may fit into the known mechanisms of intracellular Ca2+ release, and propose two models to explain the experimental data.
海星卵母细胞在减数分裂成熟和受精过程中会经历大规模的细胞内 Ca2+信号转导。尽管不同细胞环境中 Ca2+动员的引发刺激可能不同，但最终的杠杆作用通常是 Ca2+释放的第二信使，如 InsP3、cADPr 和 NAADP。细胞内 Ca2+释放的一般方案是，这些分子的相应受体作为离子通道，将游离 Ca2+从其内部储存库（如内质网腔）中释放出来。然而，越来越多的证据表明，细胞内 Ca2+释放可以被肌动球蛋白细胞骨架强烈调节。尽管已知 Ca2+有助于肌动球蛋白细胞骨架的重塑，但肌动球蛋白细胞骨架是否反过来调节 Ca2+信号尚未得到广泛探索。一个新兴的候选者可以回答 Ca2+和肌动球蛋白细胞骨架的这种相互因果关系，这个候选者可能是肌动蛋白结合蛋白。在这篇综述中，我们讨论了肌动球蛋白细胞骨架如何适应已知的细胞内 Ca2+释放机制，并提出了两个模型来解释实验数据。
