Alexandre H, Van Cauwenberge A, Mulnard J
Laboratoire de Cytologie et Embryologie moléculaires, Université libre de Bruxelles, Faculté des Sciences, Rhode-St-Genese, Belgium.
Dev Biol. 1989 Dec;136(2):311-20. doi: 10.1016/0012-1606(89)90258-3.
We confirm that the centrifugal migration of the chromosomes in maturing mouse oocytes depends on a microfilament-mediated process. We investigated the role of the cytoskeleton in the germinal vesicle (GV) behavior of oocytes prevented from resuming meiosis by either activators of protein kinase A or activators of protein kinase C. A time-lapse microcinematography study demonstrates that GV immobilization by isobutylmethylxanthine (IBMX) is overcome by colcemid (COL), nocodazole (NOC), and taxol and that cytochalasin D (CCD) reversibly immobilizes the GV of oocytes treated with either IBMX + COL (or NOC) or 12-O-tetradecanoylphorbol-13-acetate (TPA), an activator of protein kinase C, known to allow a programmed GV cortical translocation. An immunofluorescence analysis shows that the disorganization of a perinuclear microtubule network is the very first cytological clue of maturation. IBMX promotes its persistence while NOC, COL, and taxol induce its immediate disappearance. It is concluded that elements of the cytoplasmic microtubular complex (CMTC) are passively involved in the control of the setting up of a "centrifugal displacement property" (CDP) by counteracting a motive force provided by the microfilament cytoskeleton. Finally, TPA induces a clearcut reorganization instead of a total disorganization of the CMTC. This reorganization is, however, sufficient to allow the microfilaments to drive the GV displacement.
我们证实，成熟小鼠卵母细胞中染色体的离心迁移依赖于微丝介导的过程。我们研究了细胞骨架在通过蛋白激酶A激活剂或蛋白激酶C激活剂阻止恢复减数分裂的卵母细胞生发泡（GV）行为中的作用。一项延时显微电影摄影研究表明，异丁基甲基黄嘌呤（IBMX）导致的GV固定可被秋水仙酰胺（COL）、诺考达唑（NOC）和紫杉醇克服，并且细胞松弛素D（CCD）可使经IBMX + COL（或NOC）或12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA，一种蛋白激酶C激活剂，已知可使GV进行程序性皮质移位）处理的卵母细胞的GV可逆性固定。免疫荧光分析表明，核周微管网络的紊乱是成熟的首个细胞学线索。IBMX促进其持续存在，而NOC、COL和紫杉醇则导致其立即消失。得出的结论是，细胞质微管复合体（CMTC）的成分通过抵消微丝细胞骨架提供的驱动力，被动地参与“离心位移特性”（CDP）建立的控制。最后，TPA诱导CMTC发生明显的重组而非完全紊乱。然而，这种重组足以使微丝驱动GV移位。
