Two main systems regulate the plasmalemma tension and provide a close connection of the protoplast with the cell wall in fungi: turgor pressure and actin cytoskeleton. These systems work together with the plasmalemma focal adhesion to the cell wall and their contribution to fungal cell organization has been partially studied, but remains controversial in model filamentous ascomycetes and oomycetes, and even less investigated in filamentous basidiomycetes. Early endocytosis, in which F-actin is actively involved, can be used to research of mechanisms regulating the plasmalemma tension, since the latter influences on the primary endocytic vesicles formation. This study examined the effects of actin polymerization inhibitors and hyperosmotic shock on early endocytosis and cell morphology in two filamentous basidiomycetes. The main obtained results: (i) depolymerization of F-actin leads to the fast formation of primary endocytic vesicles but to inhibition of their scission; (ii) moderate hyperosmotic shock does not affect the dynamics of early endocytosis. These and a number of other results allowed offering a curtain model of regulation the plasmalemma tension in basidiomycetes. According to this model, the plasmalemma tension in many nonapical cells of hyphae is more often regulated not by turgor pressure, but by a system of actin driver cables that are associated with the proteins of focal adhesion sites. The change in the plasmalemma tension occurs similar to the movement of the curtain along the curtain rod using the curtain drivers. This model addresses the fundamental properties of the fungal structure and physiology and requires confirmation, including through the yet technically unavailable high quality labeling of the actin cytoskeleton of basidiomycetes.

中文翻译：

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早期内吞作用是了解丝状真菌质膜张力调节机制的关键

两个主要系统调节质膜张力，并提供原生质体与真菌细胞壁的紧密连接：膨胀压力和肌动蛋白细胞骨架。这些系统与质膜局灶性粘附到细胞壁上一起工作，并且它们对真菌细胞组织的贡献已经得到了部分研究，但是在模型丝状子囊菌和卵菌中仍然有争议，在丝状担子菌中的研究更少。F-肌动蛋白活跃参与的早期胞吞作用可用于研究调节质膜张力的机制，因为后者影响初级内吞囊泡的形成。这项研究检查了肌动蛋白聚合抑制剂和高渗休克对两种丝状担子菌早期内吞作用和细胞形态的影响。主要取得的结果：（i）F-肌动蛋白的解聚导致初级内吞囊泡的快速形成，但抑制了其分裂；（ii）中度高渗性休克不影响早期内吞作用的动力学。这些以及许多其他结果为调节担子菌的血浆膜张力提供了一个幕后模型。根据该模型，菌丝的许多非顶细胞中的质膜张力通常不是由膨胀压力调节，而是由与粘着斑部位蛋白相关的肌动蛋白驱动器电缆系统调节。等离子张力的变化类似于使用窗帘驱动器沿着窗帘杆沿窗帘杆的移动那样发生。该模型解决了真菌结构和生理学的基本特性，需要进行确认，