过剩基因座蛋白 4 可调节内质网功能并保持卵母细胞质量。

IF 3.4 3区 生物学 Q3 CELL BIOLOGY Cell Cycle Pub Date : 2024-03-01 Epub Date: 2024-05-31 DOI:10.1080/15384101.2024.2360287
Yuanyuan Li, Li-Quan Zhou, Ying Yin
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引用次数: 0

摘要

Surfeit locus protein 4 是一种货物受体,介导从内质网腔到高尔基体的货物运输。Surf4基因缺失会导致小鼠胚胎死亡。然而,Surf4在卵母细胞发育过程中的作用仍然未知。在这项研究中,我们建立了卵母细胞特异性敲除Surf4基因的小鼠模型。我们发现,缺失Surf4的成年小鼠卵泡生成、排卵和生育能力正常。然而,Surf4 基因缺失会轻微影响卵母细胞质量,从而导致部分卵母细胞减数分裂停滞和囊胚形成率降低。与此相一致,Surf4 缺失的小鼠卵母细胞中内质网的分布也受到干扰。这些结果表明,虽然Surf4对雌性小鼠的生育能力是不可或缺的,但Surf4能调节内质网的排列,并参与调节卵母细胞的发育能力。
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Surfeit locus protein 4 modulates endoplasmic reticulum function and maintains oocyte quality.

Surfeit locus protein 4 is a cargo receptor mediating cargo transport from the endoplasmic reticulum lumen to the Golgi apparatus. Loss of Surf4 gene led to embryonic lethality in mice. However, the role of Surf4 during oocyte development remains unknown. In this study, we generated the mouse model with oocyte-specific knockout of Surf4 gene. We found that adult mice with deletion of Surf4 showed normal folliculogenesis, ovulation and fertility. However, loss of Surf4 slightly impaired oocyte quality, thus led to partial oocyte meiotic arrest and reduced ratio of blastocyst formation. Consistent with this, the distribution of endoplasmic reticulum was disturbed in Surf4-deficient oocytes in mice. These results demonstrated that although Surf4 is dispensable for female mouse fertility, Surf4 modulates endoplasmic reticulum arrangement and participates in regulation of developmental competence of oocytes.

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来源期刊
Cell Cycle
Cell Cycle 生物-细胞生物学
CiteScore
7.70
自引率
2.30%
发文量
281
审稿时长
1 months
期刊介绍: Cell Cycle is a bi-weekly peer-reviewed journal of high priority research from all areas of cell biology. Cell Cycle covers all topics from yeast to man, from DNA to function, from development to aging, from stem cells to cell senescence, from metabolism to cell death, from cancer to neurobiology, from molecular biology to therapeutics. Our goal is fast publication of outstanding research.
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