Establishment of anterior-posterior polarity in the Caenorhabditis elegans zygote requires two different processes: mechanical activity of the actin-myosin cortex and biochemical activity of partitioning-defective (PAR) proteins. Here we analyze how PARs regulate the behavior of the cortical motor protein nonmuscle myosin (NMY-2) to complement recent efforts that investigate how PARs regulate the Rho GTPase CDC-42, which in turn regulates the actin-myosin cortex. We find that PAR-3 and PAR-6 concentrate CDC-42-dependent NMY-2 in the anterior cortex, whereas PAR-2 inhibits CDC-42-dependent NMY-2 in the posterior domain by inhibiting PAR-3 and PAR-6. In addition, we find that PAR-1 and PAR-3 are necessary for inhibiting movement of NMY-2 across the cortex. PAR-1 protects NMY-2 from being moved across the cortex by forces likely originating in the cytoplasm. Meanwhile, PAR-3 stabilizes NMY-2 against PAR-2 and PAR-6 dynamics on the cortex. We find that PAR signaling fulfills two roles: localizing NMY-2 to the anterior cortex and preventing displacement of the polarized cortical actin-myosin network.

译文

秀丽隐杆线虫合子前后极性的建立需要两个不同的过程:肌动蛋白-肌球蛋白皮层的机械活性和分区缺陷(PAR)蛋白的生化活性。在这里,我们分析了PARs如何调节皮质运动蛋白非肌肉肌球蛋白(NMY-2)的行为,以补充最近的研究,即研究PARs如何调节Rho GTPase CDC-42,后者又调节肌动蛋白-肌球蛋白皮质。我们发现PAR-3和PAR-6在前皮质集中CDC-42依赖性NMY-2,而PAR-2通过抑制PAR-3和PAR-6抑制CDC-42依赖性NMY-2在后皮质。此外,我们发现PAR-1和PAR-3对于抑制NMY-2跨皮质运动是必需的。 PAR-1保护NMY-2免受可能源自细胞质的力穿过皮质移动。同时,PAR-3使NMY-2抵抗皮层上的PAR-2和PAR-6动态。我们发现,PAR信号传导起着两个作用:将NMY-2定位在前皮质,并防止极化皮质肌动蛋白-肌球蛋白网络的移位。

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