Actin cytoskeleton is crucial to support spermatogenesis in the mammalian testis. However, the molecular mechanism(s) underlying changes of actin cytoskeletal organization in response to cellular events that take place across the seminiferous epithelium (e.g., self-renewal of spermatogonial stem cells, germ cell differentiation, meosis, spermiogenesis, spermiation) at specific stages of the epithelial cycle of spermatogenesis remain largely unexplored. This, at least in part, is due to the lack of suitable study models to identify the crucial regulatory proteins and to investigate how these proteins work in concert to support actin dynamics. Much of the information on the role of actin binding proteins in the literature, namely the actin bundling proteins, actin nucleation proteins and motor proteins, are either findings based on genetic models or morphological analyses. While this information is helpful to delineate the function of these proteins to support spermatogenesis, they are not helpful to identify the regulatory signaling proteins, the signaling pathways and the cascade of events to modulate actin cytoskeleton dynamics. Recent studies based on the use of toxicant models, both in vitro and in vivo, however, have bridged this gap by identifying putative regulatory and signaling proteins of actin cytoskeleton. Herein, we summarize and critically evaluate these findings. We also provide a hypothetical model by which actin cytoskeletal dynamics in Sertoli cells are regulated, which in turn supports spermatid transport across the seminiferous epithelium, and at the blood-testis barrier (BTB) during the epithelial cycle of spermatogenesis.

肌动蛋白细胞骨架对于支持哺乳动物睾丸中的精子发生至关重要。然而，肌动蛋白细胞骨架组织响应发生在生精上皮细胞事件中的分子机制（例如在精子发生的上皮循环的特定阶段，精原干细胞的自我更新、生殖细胞分化、减数分裂、精子发生、精子形成）在很大程度上仍未被探索。这至少部分是由于缺乏合适的研究模型来识别关键的调节蛋白并研究这些蛋白质如何协同工作以支持肌动蛋白动力学。文献中关于肌动蛋白结合蛋白作用的大部分信息，即肌动蛋白捆绑蛋白、肌动蛋白成核蛋白和运动蛋白，要么是基于遗传模型或形态分析的发现。虽然这些信息有助于描述这些蛋白质支持精子发生的功能，但它们无助于识别调节信号蛋白，信号通路和级联事件来调节肌动蛋白细胞骨架动力学。最近的研究基于使用毒物模型，然而，在体外和体内，通过鉴定肌动蛋白细胞骨架的推定调节和信号蛋白，弥合了这一差距。在此，我们总结并批判性地评估了这些发现。我们还提供了一个假设模型，通过该模型调节支持细胞中的肌动蛋白细胞骨架动力学，这反过来又支持精子细胞在精子发生的上皮周期中穿过生精上皮和血睾丸屏障 (BTB) 的转运。