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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Distinct pathways control recruitment and maintenance of myosin II at the cleavage furrow during cytokinesis
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Distinct pathways control recruitment and maintenance of myosin II at the cleavage furrow during cytokinesis

机译：不同的途径控制胞质分裂过程中卵裂沟处肌球蛋白II的募集和维持

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摘要

The correct localization of myosin II to the equatorial cortex is crucial for proper cell division. Here, we examine a collection of genes that cause defects in cytokinesis and reveal with live cell imaging two distinct phases of myosin II localization. Three genes in the rho1 signaling pathway, pebble (a Rho guanidine nucleotide exchange factor), rho1, and rho kinase, are required for the initial recruitment of myosin II to the equatorial cortex. This initial localization mechanism does not require F-actin or the two components of the centralspindlin complex, the mitotic kinesin pavarotti/MKLP1 and racGAP50c/CYK-4. However, F-actin, the centralspindlin complex, formin (diaphanous), and profilin (chickadee) are required to stably maintain myosin II at the furrow. In the absence of these latter genes, myosin II delocalizes from the equatorial cortex and undergoes highly dynamic appearances and disappearances around the entire cell cortex, sometimes associated with abnormal contractions or blebbing. Our findings support a model in which a rho kinase-dependent event, possibly myosin II regulatory light chain phosphorylation, is required for the initial recruitment to the furrow, whereas the assembly of parallel, unbranched actin filaments, generated by formin-mediated actin nucleation, is required for maintaining myosin II exclusively at the equatorial cortex.
机译：肌球蛋白II在赤道皮质的正确定位对于正确的细胞分裂至关重要。在这里，我们检查了导致胞质分裂缺陷的基因集合，并通过活细胞成像揭示了肌球蛋白II定位的两个不同阶段。肌球蛋白II最初募集到赤道皮质需要rho1信号通路中的三个基因，卵石（Rho胍核苷酸交换因子），rho1和rho激酶。这种最初的定位机制不需要F-肌动蛋白或Centralspindlin复合体的两个成分，即有丝分裂驱动蛋白pavarotti / MKLP1和racGAP50c / CYK-4。但是，需要F-肌动蛋白，中央spindlin复合体，formin（透辉）和profilin（山雀）来稳定将肌球蛋白II维持在沟中。在缺少这些基因的情况下，肌球蛋白II会从赤道皮层移离，并在整个细胞皮层周围出现高度动态的外观和消失，有时与异常的收缩或起泡有关。我们的发现支持一种模型，在该模型中，rho激酶依赖性事件（可能是肌球蛋白II调节性轻链磷酸化）是最初募集到沟中所必需的，而平行的，无支链的肌动蛋白丝的组装是由福尔明介导的肌动蛋白成核而产生的，仅在赤道皮层维持肌球蛋白II是必需的。

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