Cowan Carrie R, Hyman Anthony A
Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany.
Annu Rev Cell Dev Biol. 2004;20:427-53. doi: 10.1146/annurev.cellbio.19.111301.113823.
The one-cell Caenorhabditis elegans embryo divides asymmetrically into a larger and smaller blastomere, each with a different fate. How does such asymmetry arise? The sperm-supplied centrosome establishes an axis of polarity in the embryo that is transduced into the establishment of anterior and posterior cortical domains. These cortical domains define the polarity of the embryo, acting upstream of the PAR proteins. The PAR proteins, in turn, determine the subsequent segregation of fate determinants and the plane of cell division. We address how cortical asymmetry could be established, relying on data from C. elegans and other polarized cells, as well as from applicable models. We discuss how cortical polarity influences spindle position to accomplish an asymmetric division, presenting the current models of spindle orientation and anaphase spindle displacement. We focus on asymmetric cell division as a function of the actin and microtubule cytoskeletons, emphasizing the cell biology of polarity.
单细胞的秀丽隐杆线虫胚胎不对称分裂为一个较大和一个较小的卵裂球,每个卵裂球都有不同的命运。这种不对称是如何产生的呢?精子提供的中心体在胚胎中建立了一个极性轴,该极性轴被转化为前后皮质区域的建立。这些皮质区域定义了胚胎的极性,在PAR蛋白的上游起作用。反过来,PAR蛋白决定了命运决定因子的后续分离和细胞分裂平面。我们依据来自秀丽隐杆线虫和其他极化细胞的数据以及适用模型,探讨皮质不对称是如何建立的。我们讨论皮质极性如何影响纺锤体位置以完成不对称分裂,介绍当前的纺锤体定向模型和后期纺锤体位移模型。我们将重点放在作为肌动蛋白和微管细胞骨架功能的不对称细胞分裂上,强调极性的细胞生物学。