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Arf1 GTP酶调控卵母细胞减数分裂中高尔基体依赖性的G2/M期转换和纺锤体组织。

Arf1 GTPase Regulates Golgi-Dependent G2/M Transition and Spindle Organization in Oocyte Meiosis.

作者信息

Zhang Kun-Huan, Zou Yuan-Jing, Shan Meng-Meng, Pan Zhen-Nan, Ju Jia-Qian, Liu Jing-Cai, Ji Yi-Ming, Sun Shao-Chen

机构信息

College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China.

出版信息

Adv Sci (Weinh). 2024 Jan;11(4):e2303009. doi: 10.1002/advs.202303009. Epub 2023 Nov 28.

Abstract

ADP-ribosylation factor 1 (Arf1) is a small GTPase belonging to the Arf family. As a molecular switch, Arf1 is found to regulate retrograde and intra-Golgi transport, plasma membrane signaling, and organelle function during mitosis. This study aimed to explore the noncanonical roles of Arf1 in cell cycle regulation and cytoskeleton dynamics in meiosis with a mouse oocyte model. Arf1 accumulated in microtubules during oocyte meiosis, and the depletion of Arf1 led to the failure of polar body extrusion. Unlike mitosis, it finds that Arf1 affected Myt1 activity for cyclin B1/CDK1-based G2/M transition, which disturbed oocyte meiotic resumption. Besides, Arf1 modulated GM130 for the dynamic changes in the Golgi apparatus and Rab35-based vesicle transport during meiosis. Moreover, Arf1 is associated with Ran GTPase for TPX2 expression, further regulating the Aurora A-polo-like kinase 1 pathway for meiotic spindle assembly and microtubule stability in oocytes. Further, exogenous Arf1 mRNA supplementation can significantly rescue these defects. In conclusion, results reported the noncanonical functions of Arf1 in G2/M transition and meiotic spindle organization in mouse oocytes.

摘要

ADP-核糖基化因子1(Arf1)是一种属于Arf家族的小GTP酶。作为一种分子开关,Arf1被发现可调节有丝分裂期间的逆行和高尔基体内运输、质膜信号传导以及细胞器功能。本研究旨在利用小鼠卵母细胞模型探索Arf1在减数分裂中细胞周期调控和细胞骨架动力学方面的非经典作用。在卵母细胞减数分裂过程中,Arf1在微管中积累,Arf1的缺失导致极体排出失败。与有丝分裂不同的是,研究发现Arf1影响基于细胞周期蛋白B1/周期蛋白依赖性激酶1的G2/M期转换的Myt1活性,这干扰了卵母细胞减数分裂的恢复。此外,Arf1调节GM130以促进减数分裂期间高尔基体的动态变化和基于Rab35的囊泡运输。而且,Arf1与Ran GTP酶相关以促进TPX2表达,进而调节Aurora A-极光激酶1通路以促进卵母细胞减数分裂纺锤体组装和微管稳定性。此外,外源性补充Arf1 mRNA可显著挽救这些缺陷。总之,研究结果报道了Arf1在小鼠卵母细胞G2/M期转换和减数分裂纺锤体组织中的非经典功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f685/10811507/f5dc167b699f/ADVS-11-2303009-g005.jpg

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