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Maternal Ezh1/2 deficiency impairs the function of mitochondria in mouse oocytes and early embryos.

التفاصيل البيبلوغرافية
العنوان: Maternal Ezh1/2 deficiency impairs the function of mitochondria in mouse oocytes and early embryos.
المؤلفون: Zhang D; School of Pharmaceutical Sciences, Fujian Provincial Key Laboratory of Innovative Drug Target Research, Xiamen University, Xiamen, Fujian, China., Deng W; Fujian Provincial Key Laboratory of Reproductive Health Research, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, China., Jiang T; School of Pharmaceutical Sciences, Fujian Provincial Key Laboratory of Innovative Drug Target Research, Xiamen University, Xiamen, Fujian, China., Zhao Y; School of Pharmaceutical Sciences, Fujian Provincial Key Laboratory of Innovative Drug Target Research, Xiamen University, Xiamen, Fujian, China., Bai D; Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China., Tian Y; School of Pharmaceutical Sciences, Fujian Provincial Key Laboratory of Innovative Drug Target Research, Xiamen University, Xiamen, Fujian, China., Kong S; Fujian Provincial Key Laboratory of Reproductive Health Research, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, China., Zhang L; Fujian Provincial Key Laboratory of Reproductive Health Research, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, China., Wang H; Fujian Provincial Key Laboratory of Reproductive Health Research, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, China., Gao S; Shanghai Key Laboratory of Signaling and Disease Research, School of Life Sciences and Technology, Tongji University, Shanghai, China., Lu Z; School of Pharmaceutical Sciences, Fujian Provincial Key Laboratory of Innovative Drug Target Research, Xiamen University, Xiamen, Fujian, China.; Fujian Provincial Key Laboratory of Reproductive Health Research, Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, China.
المصدر: Journal of cellular physiology [J Cell Physiol] 2024 Jun; Vol. 239 (6), pp. e31244. Date of Electronic Publication: 2024 Mar 26.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Wiley-Liss Country of Publication: United States NLM ID: 0050222 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4652 (Electronic) Linking ISSN: 00219541 NLM ISO Abbreviation: J Cell Physiol Subsets: MEDLINE
أسماء مطبوعة: Publication: New York, NY : Wiley-Liss
Original Publication: Philadelphia, Wistar Institute of Anatomy and Biology.
مواضيع طبية MeSH: Mitochondria*/metabolism , Mitochondria*/pathology , Mitochondria*/genetics , Oocytes*/metabolism , Polycomb Repressive Complex 2*/metabolism , Polycomb Repressive Complex 2*/genetics, Animals ; Female ; Mice ; Apoptosis/genetics ; Autophagy/genetics ; Blastocyst/metabolism ; Embryonic Development/genetics ; Enhancer of Zeste Homolog 2 Protein/metabolism ; Enhancer of Zeste Homolog 2 Protein/genetics ; Enhancer of Zeste Homolog 2 Protein/deficiency ; Epigenesis, Genetic ; Gene Expression Regulation, Developmental ; Membrane Potential, Mitochondrial ; Mice, Knockout ; Morula/metabolism ; Oxidative Stress/genetics ; Reactive Oxygen Species/metabolism ; Histones/metabolism
مستخلص: Maternal histone methyltransferase is critical for epigenetic regulation and development of mammalian embryos by regulating histone and DNA modifications. Here, we reported a novel mechanism by revealing the critical effects of maternal Ezh1/2 deletion on mitochondria in MII oocytes and early embryos in mice. We found that Ezh1/2 knockout in mouse MII oocytes impaired the structure of mitochondria and decreased its number, but membrane potential and respiratory function of mitochondrion were increased. The similar effects of Ezh1/2 deletion have been observed in 2-cell and morula embryos, indicating that the effects of maternal Ezh1/2 deficiency on mitochondrion extend to early embryos. However, the loss of maternal Ezh1/2 resulted in a severe defect of morula: the number, membrane potential, respiratory function, and ATP production of mitochondrion dropped significantly. Content of reactive oxygen species was raised in both MII oocytes and early embryos, suggesting maternal Ezh1/2 knockout induced oxidative stress. In addition, maternal Ezh1/2 ablation interfered the autophagy in morula and blastocyst embryos. Finally, maternal Ezh1/2 deletion led to cell apoptosis in blastocyst embryos in mice. By analyzing the gene expression profile, we revealed that maternal Ezh1/2 knockout affected the expression of mitochondrial related genes in MII oocytes and early embryos. The chromatin immunoprecipitation-polymerase chain reaction assay demonstrated that Ezh1/2 directly regulated the expression of genes Fxyd6, Adpgk, Aurkb, Zfp521, Ehd3, Sgms2, Pygl, Slc1a1, and Chst12 by H3K27me3 modification. In conclusion, our study revealed the critical effect of maternal Ezh1/2 on the structure and function of mitochondria in oocytes and early embryos, and suggested a novel mechanism underlying maternal epigenetic regulation on early embryonic development through the modulation of mitochondrial status.
(© 2024 Wiley Periodicals LLC.)
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معلومات مُعتمدة: National Key Research and Development Program of China; National Natural Science Foundation of China
فهرسة مساهمة: Keywords: Ezh1; Ezh2; embryonic development
المشرفين على المادة: EC 2.1.1.43 (Enhancer of Zeste Homolog 2 Protein)
EC 2.1.1.43 (Ezh1 protein, mouse)
EC 2.1.1.43 (Ezh2 protein, mouse)
EC 2.1.1.43 (Polycomb Repressive Complex 2)
0 (Reactive Oxygen Species)
0 (Histones)
تواريخ الأحداث: Date Created: 20240326 Date Completed: 20240613 Latest Revision: 20240618
رمز التحديث: 20240618
DOI: 10.1002/jcp.31244
PMID: 38529784
قاعدة البيانات: MEDLINE
الوصف
تدمد:1097-4652
DOI:10.1002/jcp.31244