Distinct roles of two myosins in C. elegans spermatid differentiation
Distinct roles of two myosins in C. elegans spermatid differentiation
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两种肌球蛋白在秀丽隐杆线虫精子细胞分化中的不同作用
DOI：
10.1371/journal.pbio.3000211
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发表时间：
2019-04-01
期刊：
影响因子：
9.8
通讯作者：
Wang, Xiaochen
中科院分区：
文献类型：
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作者：
Hu, Junyan;Cheng, Shiya;Wang, Xiaochen
在精子发生过程中，相互连接的单倍体精子细胞在脱离残留体之前将不需要的细胞内容物分离成残留体(RB)。目前尚不清楚这种分化过程是如何控制的，以产生单个精子细胞或可活动的精子。在这里，我们开发了一个实时成像系统来可视化和研究线虫的这一过程。我们发现，非肌肉肌球蛋白2(nMy-2)/肌球蛋白II驱动不完全的胞质分裂产生连接的单倍体精子细胞，然后在肌球蛋白II和肌球蛋白VI的控制下极化，将不需要的细胞内容分离到RBS中。nMy-2/Myosin II从两个单倍体精子细胞之间形成的假分裂沟延伸到精子细胞极，从而促进Rb的扩张。与此同时，精子发生缺陷15(SPE-15)/肌球蛋白VI从精子细胞向扩张的Rb迁移，以促进精子细胞的萌发。肌球蛋白II或肌球蛋白VI的丢失会导致明显的细胞质分离缺陷，而这两种肌球蛋白的丢失则完全阻止Rb的形成。我们发现，RBS精子细胞的最终分离是通过肌球蛋白VI介导的胞质分裂实现的，而肌球蛋白II在这一步骤中是必不可少的。SPE-15/肌球蛋白VI和F-肌动蛋白形成一个耐洗涤剂的肌球蛋白VI环，该环经历持续的收缩，促进精子细胞和Rb之间的膜收缩。我们进一步发现RGS-GAIP相互作用蛋白C末端(GIPC)-1和GIPC-2与肌球蛋白VI协同调节收缩环的形成和精子细胞的释放。我们的研究揭示了肌球蛋白II和肌球蛋白VI在精子细胞分化中的不同作用，并发现了一种新的肌球蛋白VI介导的胞质分裂过程，控制精子细胞的释放。
During spermatogenesis, interconnected haploid spermatids segregate undesired cellular contents into residual bodies (RBs) before detaching from RBs. It is unclear how this differentiation process is controlled to produce individual spermatids or motile spermatozoa. Here, we developed a live imaging system to visualize and investigate this process in C. elegans. We found that non-muscle myosin 2 (NMY-2)/myosin II drives incomplete cytokinesis to generate connected haploid spermatids, which are then polarized to segregate undesired cellular contents into RBs under the control of myosin II and myosin VI. NMY-2/myosin II extends from the pseudo-cleavage furrow formed between two haploid spermatids to the spermatid poles, thus promoting RB expansion. In the meantime, defective spermatogenesis 15 (SPE-15)/myosin VI migrates from spermatids towards the expanding RB to promote spermatid budding. Loss of myosin II or myosin VI causes distinct cytoplasm segregation defects, while loss of both myosins completely blocks RB formation. We found that the final separation of spermatids from RBs is achieved through myosin VI–mediated cytokinesis, while myosin II is dispensable at this step. SPE-15/myosin VI and F-actin form a detergent-resistant actomyosin VI ring that undergoes continuous contraction to promote membrane constriction between spermatid and RB. We further identified that RGS-GAIP-interacting protein C terminus (GIPC)-1 and GIPC-2 cooperate with myosin VI to regulate contractile ring formation and spermatid release. Our study reveals distinct roles of myosin II and myosin VI in spermatid differentiation and uncovers a novel myosin VI–mediated cytokinesis process that controls spermatid release.