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Comparative proteomic analysis of proteins involved in oocyte meiotic maturation in mice
Author(s) -
Cao Senyang,
Guo Xuejiang,
Zhou Zuomin,
Sha Jiahao
Publication year - 2012
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.22044
Subject(s) - biology , oocyte , germinal vesicle , meiosis , polycystic ovary , microbiology and biotechnology , genetics , embryogenesis , andrology , embryo , endocrinology , gene , medicine , insulin resistance , insulin
After birth, oocytes stay at the diplotene stage in prophase of meiosis I. Meiosis resumes about 1 day before ovulation, and arrests in metaphase II (MII) after ovulation. The mature, MII oocytes are then ready for fertilization and to provide materials for early embryonic development. Proteomic characterization of oocytes can help identify proteins that are important for female meiotic maturation and early embryonic development. In this study, we compared the proteomic profiles between the germinal vesicle and MII mouse oocytes by two‐dimensional electrophoresis; 95 differentially expressed protein spots corresponding to 63 proteins were identified. Many of these proteins are known to be essential for oocyte meiosis and early embryonic development, such as adenylosuccinate synthetase, nucleoplasmin‐2, and protein–arginine deiminase type‐6. Of the 12 proteins that were identified and are highly expressed in oocytes, a novel protein, E330034G19Rik, was found to be oocyte‐specific. According to analysis by bioinformatics, it may regulate chromosome segregation during meiosis or cleavage. An in‐depth study of these proteins will help us better understand the mechanisms of oocyte meiotic maturation, fertilization, and early embryogenesis. It will also help us understand the mechanisms of diseases that stem from abnormal oocyte maturation, such as polycystic ovary syndrome and premature ovary failure. Mol. Reprod. Dev. 79:413–422, 2012. © 2012 Wiley Periodicals, Inc.