The function of myosin II in NRK cells division was investigated. Myosin II inhibitor was released at metaphase and anaphase separately. The micro-images of NRK cells in division were collected in time series. The morphology of the intercellular bridge was analyzed quantitatively by image processing software. The distribution of actin was examined using immunoflu-orescence method. Our results show that inhibition of myosin II activity resulted in karyokinesis delay or failure and lose of the polarity of daughter cells, but the progress of cytokinesis was not affected. The relative intercellular bridge diameters in myosin II inhibition group had a faster decrease than those in the controls in early cytokinesis. There was no difference in late cytokinesis. Immunofluorescence microscopy reveals that high concentration of actin filaments were present in the equatorial regions in cells treated with myosin II inhibitor as well as the control, indicating that myosin II played an important role in karyokinesis and maintenance of daughter cell polarity, but actin accumulation in the furrow did not require myosin II participation. The cytokinesis mode of NRK cells was altered in absence of myosin II.%研究肌球蛋白Ⅱ在NRK细胞分裂中的作用.分别于分裂中期和后期施加肌球蛋白Ⅱ抑制剂,对细胞分裂进行动态图像采集,采用显微图像分析软件对细胞间桥形态学进行测量分析,采用细胞免疫荧光技术检测肌动蛋白的分布,研完表明:抑制肌球蛋白Ⅱ可引起NRK细胞核分裂受阻或延迟,使子细胞丧失极性,但不影响胞质分裂进程；在胞质分裂早期,抑制肌球蛋白Ⅱ使分裂沟相对直径迅速变细,曲线明显变陡,胞质分裂晚期各组无明显差别.肌球蛋白Ⅱ抑制组与对照组分裂沟处均有肌动蛋白分布,提示肌球蛋白Ⅱ参与了细胞核分裂和子细胞极性的维持,但不影响肌动蛋白在分裂沟定位.在肌球蛋白Ⅱ爱抑制的情况下,NRK细胞胞质分裂模式发生了改变.
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