Small Lawrence E, Dawes Adriana T
Department of Molecular Genetics, The Ohio State University, Columbus, OH 43210.
Department of Molecular Genetics, The Ohio State University, Columbus, OH 43210
Mol Biol Cell. 2017 Aug 1;28(16):2220-2231. doi: 10.1091/mbc.E16-04-0263. Epub 2017 Jun 14.
Establishment of anterior-posterior polarity in the 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.
肌动蛋白-肌球蛋白皮质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,以补充最近关于PARs如何调节Rho GTPase CDC-42的研究,而CDC-42反过来又调节肌动蛋白-肌球蛋白皮质。我们发现PAR-3和PAR-6将依赖CDC-42的NMY-2集中在前皮质,而PAR-2通过抑制PAR-3和PAR-6在后区抑制依赖CDC-42的NMY-2。此外,我们发现PAR-1和PAR-3对于抑制NMY-2在皮质上的移动是必要的。PAR-1保护NMY-2不被可能起源于细胞质的力移动穿过皮质。同时,PAR-3使NMY-2在皮质上免受PAR-2和PAR-6动态变化的影响。我们发现PAR信号发挥两个作用:将NMY-2定位到前皮质,并防止极化的皮质肌动蛋白-肌球蛋白网络移位。