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Spastin interacts with CRMP5 to promote spindle organization in mouse oocytes by severing microtubules
Zygote ( IF 1.5 ) Pub Date : 2021-05-26 , DOI: 10.1017/s0967199421000344
Zhen Jin 1 , Hua-Feng Shou 2 , Jin-Wei Liu 2 , Shan-Shan Jiang 2 , Yan Shen 2 , Wei-Ye Cheng 2 , Lei-Lei Gao 2
Affiliation  

Microtubule-severing protein (MTSP) is critical for the survival of both mitotic and postmitotic cells. However, the study of MTSP during meiosis of mammalian oocytes has not been reported. We found that spastin, a member of the MTSP family, was highly expressed in oocytes and aggregated in spindle microtubules. After knocking down spastin by specific siRNA, the spindle microtubule density of meiotic oocytes decreased significantly. When the oocytes were cultured in vitro, the oocytes lacking spastin showed an obvious maturation disorder. Considering the microtubule-severing activity of spastin, we speculate that spastin on spindles may increase the number of microtubule broken ends by severing the microtubules, therefore playing a nucleating role, promoting spindle assembly and ensuring normal meiosis. In addition, we found the colocalization and interaction of collapsin response mediator protein 5 (CRMP5) and spastin in oocytes. CRMP5 can provide structural support and promote microtubule aggregation, creating transportation routes, and can interact with spastin in the microtubule activity of nerve cells (30). Knocking down CRMP5 may lead to spindle abnormalities and developmental disorders in oocytes. Overexpression of spastin may reverse the abnormal phenotype caused by the deletion of CRMP5. In summary, our data support a model in which the interaction between spastin and CRMP5 promotes the assembly of spindle microtubules in oocytes by controlling microtubule dynamics, therefore ensuring normal meiosis.

中文翻译:

Spastin 与 CRMP5 相互作用,通过切断微管促进小鼠卵母细胞中的纺锤体组织

微管切断蛋白 (MTSP) 对于有丝分裂和有丝分裂后细胞的存活都至关重要。然而,尚未报道哺乳动物卵母细胞减数分裂期间MTSP的研究。我们发现作为 MTSP 家族成员的 spastin 在卵母细胞中高度表达并在纺锤体微管中聚集。特异性siRNA敲除spastin后,减数分裂卵母细胞的纺锤体微管密度显着降低。卵母细胞培养时体外, 缺乏 spastin 的卵母细胞表现出明显的成熟障碍。考虑到 spastin 的微管切断活性,我们推测纺锤体上的 spastin 可能通过切断微管增加微管断端的数量,从而发挥成核作用,促进纺锤体组装,确保正常的减数分裂。此外,我们在卵母细胞中发现了 collapsin 反应介质蛋白 5 (CRMP5) 和 spastin 的共定位和相互作用。CRMP5 可以提供结构支持和促进微管聚集,创造运输路线,并且可以在神经细胞的微管活动中与 spastin 相互作用 (30)。敲低 CRMP5 可能导致卵母细胞的纺锤体异常和发育障碍。spastin的过表达可能会逆转CRMP5缺失引起的异常表型。总之,
更新日期:2021-05-26
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