Chowdhury Pritha, Sinha Debatrayee, Poddar Abhishek, Chetluru Madhurya, Chen Qian
bioRxiv. 2024 Apr 6:2024.01.15.575753. doi: 10.1101/2024.01.15.575753.
Cytokinesis, the last step in cell division, separate daughter cells through the force produced by an actomyosin contractile ring assembled at the equatorial plane. In fission yeast cells, the ring helps recruit a mechanosensitive ion channel Pkd2 to the cleavage furrow, whose activation by membrane tension promotes calcium influx and daughter cell separation. However, it is unclear how the activities of Pkd2 may affect the actomyosin ring. Here, through both microscopic and genetic analyses of a hypomorphic mutant of the essential gene, we examine its potential role in assembling and constricting the contractile ring. The mutation significantly increased the number of type II myosin heavy chain Myo2 (+20%), its regulatory light chain Rlc1 (+37%) and actin (+20%) molecules in the ring, compared to the wild type. Consistent with a regulatory role of Pkd2 in the ring assembly, we identified a strong negative genetic interaction between and the temperature-sensitive mutant . The cells often failed to assemble a complete contractile ring. We conclude that Pkd2 modulates the recruitment of type II myosin and actin to the contractile ring, suggesting a novel calcium- dependent mechanism regulating the actin cytoskeletal structures during cytokinesis.
胞质分裂是细胞分裂的最后一步，通过在赤道平面组装的肌动球蛋白收缩环产生的力来分离子细胞。在裂殖酵母细胞中，该环有助于将机械敏感离子通道Pkd2募集到分裂沟，膜张力对其激活可促进钙内流和子细胞分离。然而，尚不清楚Pkd2的活性如何影响肌动球蛋白环。在这里，通过对必需基因的一个亚效突变体进行显微镜和遗传学分析，我们研究了它在组装和收缩收缩环中的潜在作用。与野生型相比，该突变显著增加了环中II型肌球蛋白重链Myo2（增加20%）、其调节轻链Rlc1（增加37%）和肌动蛋白（增加20%）分子的数量。与Pkd2在环组装中的调节作用一致，我们确定了它与温度敏感突变体之间存在强烈的负遗传相互作用。该突变体细胞常常无法组装完整的收缩环。我们得出结论，Pkd2调节II型肌球蛋白和肌动蛋白向收缩环的募集，提示了一种在胞质分裂过程中调节肌动蛋白细胞骨架结构的新型钙依赖机制。
