scholarly journals The cyclin B2/CDK1 complex inhibits separase activity in mouse oocyte meiosis I

Development ◽  
2019 ◽  
Vol 146 (23) ◽  
pp. dev182519 ◽  
Author(s):  
Jian Li ◽  
Ying-Chun Ouyang ◽  
Chun-Hui Zhang ◽  
Wei-Ping Qian ◽  
Qing-Yuan Sun
Keyword(s):  
Mouse Oocyte ◽  
Oocyte Meiosis ◽  
Meiosis I

scholarly journals Mps1 kinase-dependent Sgo2 centromere localisation mediates cohesin protection in mouse oocyte meiosis I

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Warif El Yakoubi ◽  
Eulalie Buffin ◽  
Damien Cladière ◽  
Yulia Gryaznova ◽  
Inés Berenguer ◽  
...  
Keyword(s):  
Mouse Oocyte ◽  
Oocyte Meiosis ◽  
Meiosis I

scholarly journals The Cyclin B2/CDK1 Complex Conservatively Inhibits Separase Activity in Oocyte Meiosis II

2021 ◽  
Vol 9 ◽  
Author(s):  
Jian Li ◽  
Hong-Yong Zhang ◽  
Feng Wang ◽  
Qing-Yuan Sun ◽  
Wei-Ping Qian
Keyword(s):  
Chromosome Segregation ◽  
Homologous Chromosome ◽  
Cyclin B1 ◽  
Mouse Oocyte ◽  
Parthenogenetic Activation ◽  
Sister Chromatids ◽  
Oocyte Meiosis ◽  
Meiosis I

Recently, we have reported that the cyclin B2/CDK1 complex regulates homologous chromosome segregation through inhibiting separase activity in oocyte meiosis I, which further elucidates the compensation of cyclin B2 on cyclin B1’s function in meiosis I. However, whether cyclin B2/CDK1 complex also negatively regulates separase activity during oocyte meiosis II remains unknown. In the present study, we investigated the function of cyclin B2 in meiosis II of oocyte. We found that stable cyclin B2 expression impeded segregation of sister chromatids after oocyte parthenogenetic activation. Consistently, stable cyclin B2 inhibited separase activation, while introduction of non-phosphorylatable separase mutant rescued chromatid separation in the stable cyclin B2-expressed oocytes. Therefore, the cyclin B2/CDK1 complex conservatively regulates separase activity via inhibitory phosphorylation of separase in both meiosis I and meiosis II of mouse oocyte.

scholarly journals MCAK regulates chromosome alignment but is not necessary for preventing aneuploidy in mouse oocyte meiosis I

Development ◽  
2010 ◽  
Vol 137 (13) ◽  
pp. 2133-2138 ◽  
Author(s):  
C. Illingworth ◽  
N. Pirmadjid ◽  
P. Serhal ◽  
K. Howe ◽  
G. FitzHarris
Keyword(s):  
Mouse Oocyte ◽  
Oocyte Meiosis ◽  
Chromosome Alignment ◽  
Meiosis I

scholarly journals Ral GTPase is essential for actin dynamics and Golgi apparatus distribution in mouse oocyte maturation

Cell Division ◽  
2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Ming-Hong Sun ◽  
Lin-Lin Hu ◽  
Chao-Ying Zhao ◽  
Xiang Lu ◽  
Yan-Ping Ren ◽  
...  
Keyword(s):  
Golgi Apparatus ◽  
Oocyte Maturation ◽  
Polar Body ◽  
Mouse Oocyte ◽  
Actin Dynamics ◽  
Mouse Oocytes ◽  
Oocyte Meiosis ◽  
Ral Gtpase ◽  
Polar Body Extrusion ◽  
Cytoskeleton Dynamics

Abstract Background Ral family is a member of Ras-like GTPase superfamily, which includes RalA and RalB. RalA/B play important roles in many cell biological functions, including cytoskeleton dynamics, cell division, membrane transport, gene expression and signal transduction. However, whether RalA/B involve into the mammalian oocyte meiosis is still unclear. This study aimed to explore the roles of RalA/B during mouse oocyte maturation. Results Our results showed that RalA/B expressed at all stages of oocyte maturation, and they were enriched at the spindle periphery area after meiosis resumption. The injection of RalA/B siRNAs into the oocytes significantly disturbed the polar body extrusion, indicating the essential roles of RalA/B for oocyte maturation. We observed that in the RalA/B knockdown oocytes the actin filament fluorescence intensity was significantly increased at the both cortex and cytoplasm, and the chromosomes were failed to locate near the cortex, indicating that RalA/B regulate actin dynamics for spindle migration in mouse oocytes. Moreover, we also found that the Golgi apparatus distribution at the spindle periphery was disturbed after RalA/B depletion. Conclusions In summary, our results indicated that RalA/B affect actin dynamics for chromosome positioning and Golgi apparatus distribution in mouse oocytes.

FASCIN regulates actin assembly for spindle movement and polar body extrusion in mouse oocyte meiosis

2021 ◽  
Author(s):  
Lin‐Lin Hu ◽  
Meng‐Hao Pan ◽  
Feng‐Lian Yang ◽  
Zi‐Ao Zong ◽  
Feng Tang ◽  
...  
Keyword(s):  
Polar Body ◽  
Mouse Oocyte ◽  
Actin Assembly ◽  
Oocyte Meiosis ◽  
Polar Body Extrusion

scholarly journals OLA1 is responsible for normal spindle assembly and SAC activation in mouse oocytes

2019 ◽  
Author(s):  
Di Xie ◽  
Juan Zhang ◽  
JinLi Ding ◽  
Jing Yang ◽  
Yan Zhang
Keyword(s):  
Spindle Assembly Checkpoint ◽  
Polar Body ◽  
Germinal Vesicle ◽  
Spindle Assembly ◽  
Mouse Oocyte ◽  
Immunofluorescent Staining ◽  
Germinal Vesicle Breakdown ◽  
Oocyte Meiosis ◽  
Polar Body Extrusion ◽  
Spread Analysis

Background. OLA1 is a member of the GTPase protein family, unlike other members, it can bind and hydrolyze ATP more efficiently than GTP. OLA1 participates in cell proliferation, oxidative response and tumorigenesis. However, whether OLA1 is also required for oocyte meiosis is still unknown. Methods. In this study, the localization, expression, and functions of OLA1 in the mouse oocyte meiosis were examined. Immunofluorescent and confocal microscopy were used to explore the location pattern of OLA1 in the mouse oocyte. Moreover, nocodazole treatment was used to confirm the spindle-like location of OLA1 during mouse meiosis. Western blot was used to explore the expression pattern of OLA1 in the mouse oocyte. Microinjection of siRNA was used to explore the OLA1 functions in the mouse oocyte meiosis. In addition, chromosome spreading was used to investigate the spindle assembly checkpoint (SAC) activity. Results. Immunofluorescent staining showed that OLA1 evenly distributed in the cytoplasm at germinal vesicle (GV) stage. After meiosis resumption (GVBD), OLA1 co-localized with spindles, which was further identified by nocodazole treatment experiments. Knockdown of OLA1 impaired the germinal vesicle breakdown progression and finally resulted in a lower polar body extrusion rate. Immunofluorescence analysis indicated that knockdown of OLA1 led to abnormal spindle assembly, which was evidenced by multipolar spindles in OLA1-RNAi-oocytes. After 6 h post-GVBD in culture, an increased proportion of oocyte which has precociously entered into anaphase/telephase I (A/TI) was observed in OLA1-knockdown oocytes, suggesting that loss of OLA1 resulted in the premature segregation of homologous chromosomes. In addition, the chromosome spread analysis suggested that OLA1 knockdown induced premature anaphase onset was due to the precocious inactivation of SAC. Taken together, we concluded that OLA1 plays important role in GVBD, spindle assembly and SAC activation maintenance in oocyte meiosis.

scholarly journals Kif4 Is Essential for Mouse Oocyte Meiosis

PLoS ONE ◽  
2017 ◽  
Vol 12 (1) ◽  
pp. e0170650 ◽  
Author(s):  
Nicole J. Camlin ◽  
Eileen A. McLaughlin ◽  
Janet E. Holt
Keyword(s):  
Mouse Oocyte ◽  
Oocyte Meiosis

RAB8A GTPase regulates spindle migration and Golgi apparatus distribution via ROCK-mediated actin assembly in mouse oocyte meiosis†

2018 ◽  
Vol 100 (3) ◽  
pp. 711-720 ◽  
Author(s):  
Zhen-Nan Pan ◽  
Yujie Lu ◽  
Feng Tang ◽  
Meng-Hao Pan ◽  
Xiang Wan ◽  
...  
Keyword(s):  
Golgi Apparatus ◽  
Mouse Oocyte ◽  
Actin Assembly ◽  
Oocyte Meiosis
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