In tip-growing plant cells, growth results from myosin XI and F-actin-mediated deposition of cell wall polysaccharides contained in secretory vesicles. Previous evidence showed that myosin XI anticipates F-actin accumulation at the cell’s tip, suggesting a mechanism where vesicle clustering via myosin XI increases F-actin polymerization. To evaluate this model, we used a conditional loss-of-function strategy by generating moss (Physcomitrium patens) plants harboring a myosin XI temperature-sensitive allele. We found that loss of myosin XI function alters tip cell morphology, vacuolar homeostasis, and cell viability but not following F-actin depolymerization. Importantly, our conditional loss-of-function analysis shows that myosin XI focuses and directs vesicles at the tip of the cell, which induces formin-dependent F-actin polymerization, increasing F-actin’s local concentration. Our findings support the role of myosin XI in vesicle focusing, possibly via clustering and F-actin organization, necessary for tip growth, and deepen our understanding of additional myosin XI functions.

中文翻译：

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肌球蛋白XI通过囊泡聚焦和F-肌动蛋白在Physcommitrium patens中的局部富集来驱动极化生长

在尖端生长的植物细胞中，生长是由肌球蛋白 XI 和 F-肌动蛋白介导的分泌囊泡中所含的细胞壁多糖的沉积引起的。先前的证据表明，肌球蛋白 XI 可预测细胞尖端的 F-肌动蛋白积累，这表明通过肌球蛋白 XI 的囊泡聚集增加了 F-肌动蛋白聚合的机制。为了评估这个模型，我们使用了条件性功能丧失策略，通过生成具有肌球蛋白 XI 温度敏感等位基因的苔藓 (Physcommitrium patens) 植物。我们发现肌球蛋白 XI 功能的丧失会改变尖端细胞形态、液泡稳态和细胞活力，但不会改变 F-肌动蛋白解聚。重要的是，我们的条件性功能丧失分析表明，肌球蛋白 XI 聚焦并引导细胞尖端的囊泡，从而诱导依赖于甲酸的 F-肌动蛋白聚合，增加 F-actin 的局部浓度。我们的研究结果支持肌球蛋白 XI 在囊泡聚焦中的作用，可能通过聚集和 F-肌动蛋白组织，这是尖端生长所必需的，并加深了我们对其他肌球蛋白 XI 功能的理解。