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一种微管相关蛋白在防止卵母细胞逃避纺锤体组装检查点中发挥作用。

A Microtubule-Associated Protein Functions in Preventing Oocytes from Evading the Spindle Assembly Checkpoint.

作者信息

Zhou Changyin, Zhang Xue, Xu Genlu, Ran Yuting, Wang Hui, Xie Xuefeng, Li Ang, Li Fei, Li Xiaozhen, Ding Jinlong, Zhang Mianqun, Sun Qing-Yuan, Ou Xiang-Hong

机构信息

Guangzhou Key Laboratory of Metabolic Diseases and Reproductive Health, Guangdong-Hong Kong Metabolism & Reproduction Joint Laboratory, Reproductive Medicine Center, The Affiliated Guangdong Second Provincial General Hospital of Jinan University, Guangzhou, 510317, China.

School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, 510006, China.

出版信息

Adv Sci (Weinh). 2025 Feb;12(7):e2413097. doi: 10.1002/advs.202413097. Epub 2024 Dec 25.

DOI:10.1002/advs.202413097
PMID:39721007
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11831433/
Abstract

Aneuploidy eggs are a common cause of human infertility, spontaneous abortion, or trisomy syndromes. The spindle assembly checkpoint (SAC) plays a crucial role in preventing aneuploidy in oocytes, yet it is unclear if additional mechanisms exist to ensure oocyte adherence to this checkpoint. It is now revealed that the microtubule-associated protein NUSAP can prevent oocytes from evading the SAC and regulate the speed of the cell cycle. Mechanistically, the study identifies NUSAP as a novel stabilizer of the E3 ubiquitin ligase APC/C, protecting CDH1 from SCF-mediated degradation. Depletion of NUSAP reduces CDH1 protein level, leading to abnormal spindle assembly and chromosome alignment, and disrupting the balance of cell cycle proteins. This misregulated balance causes oocytes to evade the SAC. Consequently, these abnormal oocytes not only fail to arrest at metaphase but also accelerate the cell process, ultimately resulting in the production of aneuploid eggs. Together, the findings not only clarify the existence of mechanisms that ensure oocytes compliance with the spindle assembly checkpoint but also expand the new functions of NUSAP beyond its role as a microtubule- associated protein.

摘要

非整倍体卵子是人类不孕、自然流产或三体综合征的常见原因。纺锤体组装检查点（SAC）在防止卵母细胞出现非整倍体方面起着关键作用，但尚不清楚是否存在其他机制来确保卵母细胞遵守这一检查点。现在有研究表明，微管相关蛋白NUSAP可以防止卵母细胞逃避SAC，并调节细胞周期的速度。从机制上讲，该研究确定NUSAP是E3泛素连接酶APC/C的一种新型稳定剂，可保护CDH1免受SCF介导的降解。NUSAP的缺失会降低CDH1蛋白水平，导致纺锤体组装和染色体排列异常，并破坏细胞周期蛋白的平衡。这种失调的平衡会导致卵母细胞逃避SAC。因此，这些异常卵母细胞不仅无法在中期停滞，还会加速细胞进程，最终产生非整倍体卵子。总之，这些发现不仅阐明了确保卵母细胞遵守纺锤体组装检查点的机制的存在，还扩展了NUSAP作为微管相关蛋白之外的新功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/50c852cde55d/ADVS-12-2413097-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/1656385f0083/ADVS-12-2413097-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/1dbbc9cd1853/ADVS-12-2413097-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/47f7e9c4c34b/ADVS-12-2413097-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/89377e735386/ADVS-12-2413097-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/9e2831ac0106/ADVS-12-2413097-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/fde47f6a71f6/ADVS-12-2413097-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/50c852cde55d/ADVS-12-2413097-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/1656385f0083/ADVS-12-2413097-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/1dbbc9cd1853/ADVS-12-2413097-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/47f7e9c4c34b/ADVS-12-2413097-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/89377e735386/ADVS-12-2413097-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/9e2831ac0106/ADVS-12-2413097-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/fde47f6a71f6/ADVS-12-2413097-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae97/11831433/50c852cde55d/ADVS-12-2413097-g005.jpg

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