scholarly journals Intrinsically Defective Microtubule Dynamics Contribute to Age-Related Chromosome Segregation Errors in Mouse Oocyte Meiosis-I

2017 ◽  
Vol 27 (7) ◽  
pp. 1040-1047 ◽  
Author(s):  
Shoma Nakagawa ◽  
Greg FitzHarris
Author(s):  
Jian Li ◽  
Hong-Yong Zhang ◽  
Feng Wang ◽  
Qing-Yuan Sun ◽  
Wei-Ping Qian

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.


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

PLoS ONE ◽  
2009 ◽  
Vol 4 (11) ◽  
pp. e7701 ◽  
Author(s):  
Mo Li ◽  
Sen Li ◽  
Ju Yuan ◽  
Zhen-Bo Wang ◽  
Shao-Chen Sun ◽  
...  

2016 ◽  
Vol 1863 (4) ◽  
pp. 630-637 ◽  
Author(s):  
Hyuk-Joon Jeon ◽  
Seung Yeop You ◽  
Yong Seok Park ◽  
Jong Wook Chang ◽  
Jae-Sung Kim ◽  
...  

Development ◽  
2010 ◽  
Vol 137 (13) ◽  
pp. 2133-2138 ◽  
Author(s):  
C. Illingworth ◽  
N. Pirmadjid ◽  
P. Serhal ◽  
K. Howe ◽  
G. FitzHarris

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

2008 ◽  
Vol 180 (3) ◽  
pp. 459-466 ◽  
Author(s):  
Jianwei Zou ◽  
Mark A. Hallen ◽  
Christine D. Yankel ◽  
Sharyn A. Endow

The kinesin-13 motor, KLP10A, destabilizes microtubules at their minus ends in mitosis and binds to polymerizing plus ends in interphase, regulating spindle and microtubule dynamics. Little is known about kinesin-13 motors in meiosis. In this study, we report that KLP10A localizes to the unusual pole bodies of anastral Drosophila melanogaster oocyte meiosis I spindles as well as spindle fibers, centromeres, and cortical microtubules. We frequently observe the pole bodies attached to cortical microtubules, indicating that KLP10A could mediate spindle anchoring to the cortex via cortical microtubules. Oocytes treated with drugs that suppress microtubule dynamics exhibit spindles that are reoriented more vertically to the cortex than untreated controls. A dominant-negative klp10A mutant shows both reoriented and shorter oocyte spindles, implying that, unexpectedly, KLP10A may stabilize rather than destabilize microtubules, regulating spindle length and positioning the oocyte spindle. By altering microtubule dynamics, KLP10A could promote spindle reorientation upon oocyte activation.


2021 ◽  
Author(s):  
Aleksandar I. Mihajlović ◽  
Jenna Haverfield ◽  
Greg FitzHarris

SUMMARYChromosome segregation errors that cause oocyte aneuploidy increase in frequency with maternal age and are considered a major contributing factor of age-related fertility decline in females. A common age-associated chromosome segregation phenomenon in oocytes is the lagging anaphase chromosome, but whether anaphase laggards actually missegregate and cause aneuploidy is unclear. Here we show unexpectedly that lagging chromosomes in mouse oocytes comprise two mechanistically distinct classes of motion that we refer to as ‘Class-I’ and ‘Class-II’. We use imaging approaches and mechanistic interventions to dissociate the two classes, and find that whereas Class-II laggards are benign, Class-I laggards can directly cause aneuploidy. Most notably, a controlled prolongation of meiosis-I specifically lessens Class-I lagging to prevent aneuploidy. Our data thus reveal lagging chromosomes to be a cause of age-related aneuploidy in mouse oocytes and suggest that manipulating the cell cycle could increase the yield of useful oocytes in some contexts.


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