Goulding Morgan B, Canman Julie C, Senning Eric N, Marcus Andrew H, Bowerman Bruce
Institute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.
J Cell Biol. 2007 Sep 24;178(7):1177-91. doi: 10.1083/jcb.200703159.
Mitotic spindle positioning in the Caenorhabditis elegans zygote involves microtubule-dependent pulling forces applied to centrosomes. In this study, we investigate the role of actomyosin in centration, the movement of the nucleus-centrosome complex (NCC) to the cell center. We find that the rate of wild-type centration depends equally on the nonmuscle myosin II NMY-2 and the Galpha proteins GOA-1/GPA-16. In centration- defective let-99(-) mutant zygotes, GOA-1/GPA-16 and NMY-2 act abnormally to oppose centration. This suggests that LET-99 determines the direction of a force on the NCC that is promoted by Galpha signaling and actomyosin. During wild-type centration, NMY-2-GFP aggregates anterior to the NCC tend to move further anterior, suggesting that actomyosin contraction could pull the NCC. In GOA-1/GPA-16-depleted zygotes, NMY-2 aggregate displacement is reduced and largely randomized, whereas in a let-99(-) mutant, NMY-2 aggregates tend to make large posterior displacements. These results suggest that Galpha signaling and LET-99 control centration by regulating polarized actomyosin contraction.
秀丽隐杆线虫受精卵中的有丝分裂纺锤体定位涉及施加于中心体的微管依赖性拉力。在本研究中，我们探究了肌动球蛋白在中心定位（即核 - 中心体复合体（NCC）向细胞中心移动）中的作用。我们发现野生型中心定位的速率同样依赖于非肌肉肌球蛋白II NMY - 2以及Gα蛋白GOA - 1/GPA - 16。在中心定位缺陷的let - 99(-)突变受精卵中，GOA - 1/GPA - 16和NMY - 2表现异常，阻碍中心定位。这表明LET - 99决定了由Gα信号传导和肌动球蛋白促进的作用于NCC的力的方向。在野生型中心定位过程中，位于NCC前方的NMY - 2 - GFP聚集体倾向于进一步向前移动，这表明肌动球蛋白收缩可能拉动NCC。在耗尽GOA - 1/GPA - 16的受精卵中，NMY - 2聚集体的位移减少且大多随机化，而在let - 99(-)突变体中，NMY - 2聚集体倾向于向后大幅位移。这些结果表明，Gα信号传导和LET - 99通过调节极化的肌动球蛋白收缩来控制中心定位。
