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The SUMO pathway functions in mouse oocyte maturation
Authors:Zhen-Bo Wang  Xiang-Hong Ou  Jing-Shan Tong  Sen Li  Liang Wei  Ying-Chun Ouyang  Yi Hou  Heide Schatten  Qing-Yuan Sun
Institution:1.State Key Laboratory of Reproductive Biology; Institute of Zoology; Chinese Academy of Sciences; Beijing, China;2.Graduate School; Chinese Academy of Sciences; Beijing, China;3.Department of Veterinary pathobiology; University of Missouri-Columbia; Mo, USA;4.Center of reproductive Medicine; Department of obstetrics and Gynecology; Nanfang Hospital; Southern Medical University; Guangzhou, China
Abstract:Sumoylation is an important posttranslational modification in which SUMO (small ubiquitin-related modifier) proteins are bonded covalently to their substrates. Studies on the roles of sumoylation in cell cycle regulation have been emerging in both mitosis from yeast to mammals and meiosis in budding yeast, but the functions of sumoylation in mammalian meiosis, especially in oocyte meiotic maturation are not well known. Here, we examined the localization and expression of SUMO-1 and SUMO-2/3, the two basic proteins in the sumoylation pathway and investigated their roles through overexpression of Senp2 during mouse oocyte maturation. Immunofluorescent staining revealed differential patterns of SUMO-1 and SUMO-2/3 localization: SUMO-1 was localized to the spindle poles in prometaphase I, MI and MII stages, around the separating homologues in anaphase I and telophase I stages of first meiosis, while SUMO-2/3 was mainly concentrated near centromeres during mouse oocyte maturation. Immunoblot analysis uncovered the different expression profiles of SUMO-1 and SUMO-2/3 modified proteins during mouse oocyte maturation. Overexpression of Senp2, a SUMO-specific isopeptidase, caused changes of SUMO-modified proteins and led to defects in MII spindle organization in mature eggs. These results suggest that the SUMO pathway may play an indispensable role during mouse oocyte meiotic maturation.Key words: sumoylation, mouse oocyte maturation, overexpression, Senp2, MII spindle
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