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

Author

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

Subjects
GOLGI apparatus, SPINDLE apparatus, CELL cycle regulation, MEIOSIS, GUANOSINE triphosphatase, OVUM
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. [ABSTRACT FROM AUTHOR]

Published
2024
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32. NAMPT regulates mitochondria function and lipid metabolism during porcine oocyte maturation.

Author

Guo, Xin, Jiao, Le, Yi, Yang, Zhang, Hao‐Lin, Liu, Ya‐Xi, Wang, Zi‐Yu, and Sun, Shao‐Chen

Subjects
LIPID metabolism, OVUM, MITOCHONDRIA, MITOCHONDRIAL DNA, TUBULINS, MEMBRANE potential, DNA repair
Abstract

Oocyte maturation defect can lead to maternal reproduction disorder. NAMPT is a rate‐limiting enzyme in mammalian NAD+ biosynthesis pathway, which can regulate a variety of cellular metabolic processes including glucose metabolism and DNA damage repair. However, the function of NAMPT in porcine oocytes remains unknown. In this study, we showed that NAMPT involved into multiple cellular events during oocyte maturation. NAMPT expressed during all stages of porcine oocyte meiosis, and inhibition of NAMPT activity caused the cumulus expansion and polar body extrusion defects. Mitochondrial dysfunction was observed in NAMPT‐deficient porcine oocytes, which showed decreased membrane potential, ATP and mitochondrial DNA content, increased oxidative stress level and apoptosis. We also found that NAMPT was essential for spindle organization and chromosome arrangement based on Ac‐tubulin. Moreover, lack of NAMPT activity caused the increase of lipid droplet and affected the imbalance of lipogenesis and lipolysis. In conclusion, our study indicated that lack of NAMPT activity affected porcine oocyte maturation through its effects on mitochondria function, spindle assembly and lipid metabolism. [ABSTRACT FROM AUTHOR]

Published
2024
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41. Acrylamide Exposure Destroys the Distribution and Functions of Organelles in Mouse Oocytes

Author

Zhao, Chao-Ying, Hu, Lin-Lin, Xing, Chun-Hua, Lu, Xiang, Sun, Shao-Chen, Wei, Yu-Xia, and Ren, Yan-Ping

Subjects
musculoskeletal diseases, immune system diseases, Cell Biology, skin and connective tissue diseases, Developmental Biology
Abstract

Acrylamide (ACR) is a common industrial ingredient which is also found in foods that are cooked at high temperatures. ACR has been shown to have multiple toxicities including reproductive toxicity. Previous studies reported that ACR caused oocyte maturation defects through the induction of apoptosis and oxidative stress. In the present study, we showed that ACR exposure affected oocyte organelle functions, which might be the reason for oocyte toxicity. We found that exposure to 5 mM ACR reduced oocyte maturation. ACR caused abnormal mitochondrial distribution away from spindle periphery and reduced mitochondrial membrane potential. Further analysis showed that ACR exposure reduced the fluorescence intensity of Rps3 and abnormal distribution of the endoplasmic reticulum, indicating that ACR affected protein synthesis and modification in mouse oocytes. We found the negative effects of ACR on the distribution of the Golgi apparatus; in addition, fluorescence intensity of vesicle transporter Rab8A decreased, suggesting the decrease in protein transport capacity of oocytes. Furthermore, the simultaneous increase in lysosomes and LAMP2 fluorescence intensity was also observed, suggesting that ACR affected protein degradation in oocytes. In conclusion, our results indicated that ACR exposure disrupted the distribution and functions of organelles, which further affected oocyte developmental competence in mice.

Published
2022

44. Additional file 1 of Regulation of paternal 5mC oxidation and H3K9me2 asymmetry by ERK1/2 in mouse zygotes

Author

Chen, Baobao, Deng, Mingtian, Pan, Meng-Hao, Sun, Shao-Chen, and Liu, Honglin

Subjects
embryonic structures, environment and public health
Abstract

Additional file 1: Figure S1. Phenotype of zygotes following treatment with inhibitors of MEK1/2, ERK1/2, p38, and JNK. Figure S2. The expression of phosphorylated and total MAPKs proteins in zygotes treated with corresponding inhibitors. Figure S3. The expression of pluripotent genes in morula that zygotic ERK1/2 inhibited. Figure S4. The expression of Dnmt1 and Dnmt3a in DNMT-inhibited zygotes.

Published
2022
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