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 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 spindle checkpoint protein Mad2 regulates APC/C activity during prometaphase and metaphase of meiosis I in Saccharomyces cerevisiae

2011 ◽  
Vol 22 (16) ◽  
pp. 2848-2861 ◽  
Author(s):  
Dai Tsuchiya ◽  
Claire Gonzalez ◽  
Soni Lacefield
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Chromosome Segregation ◽  
Meiotic Division ◽  
Spindle Checkpoint ◽  
Yeast Cells ◽  
Meiotic Cell ◽  
Checkpoint Protein ◽  
Sister Chromatids ◽  
Meiosis I

In many eukaryotes, disruption of the spindle checkpoint protein Mad2 results in an increase in meiosis I nondisjunction, suggesting that Mad2 has a conserved role in ensuring faithful chromosome segregation in meiosis. To characterize the meiotic function of Mad2, we analyzed individual budding yeast cells undergoing meiosis. We find that Mad2 sets the duration of meiosis I by regulating the activity of APCCdc20. In the absence of Mad2, most cells undergo both meiotic divisions, but securin, a substrate of the APC/C, is degraded prematurely, and prometaphase I/metaphase I is accelerated. Some mad2Δ cells have a misregulation of meiotic cell cycle events and undergo a single aberrant division in which sister chromatids separate. In these cells, both APCCdc20 and APCAma1 are prematurely active, and meiosis I and meiosis II events occur in a single meiotic division. We show that Mad2 indirectly regulates APCAma1 activity by decreasing APCCdc20 activity. We propose that Mad2 is an important meiotic cell cycle regulator that ensures the timely degradation of APC/C substrates and the proper orchestration of the meiotic divisions.

scholarly journals Shugoshin Promotes Sister Kinetochore Biorientation in Saccharomyces cerevisiae

2008 ◽  
Vol 19 (3) ◽  
pp. 1199-1209 ◽  
Author(s):  
Brendan M. Kiburz ◽  
Angelika Amon ◽  
Adele L. Marston
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Chromosome Segregation ◽  
Minor Role ◽  
Meiotic Cell ◽  
Homologous Chromosomes ◽  
Cell Divisions ◽  
Sister Chromatids ◽  
Sister Kinetochore ◽  
A Minor ◽  
Meiosis I

Chromosome segregation must be executed accurately during both mitotic and meiotic cell divisions. Sgo1 plays a key role in ensuring faithful chromosome segregation in at least two ways. During meiosis this protein regulates the removal of cohesins, the proteins that hold sister chromatids together, from chromosomes. During mitosis, Sgo1 is required for sensing the absence of tension caused by sister kinetochores not being attached to microtubules emanating from opposite poles. Here we describe a differential requirement for Sgo1 in the segregation of homologous chromosomes and sister chromatids. Sgo1 plays only a minor role in segregating homologous chromosomes at meiosis I. In contrast, Sgo1 is important to bias sister kinetochores toward biorientation. We suggest that Sgo1 acts at sister kinetochores to promote their biorientation.

scholarly journals Human securin proteolysis is controlled by the spindle checkpoint and reveals when the APC/C switches from activation by Cdc20 to Cdh1

2002 ◽  
Vol 157 (7) ◽  
pp. 1125-1137 ◽  
Author(s):  
Anja Hagting ◽  
Nicole den Elzen ◽  
Hartmut C. Vodermaier ◽  
Irene C. Waizenegger ◽  
Jan-Michael Peters ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Sister Chromatid ◽  
Live Cell Imaging ◽  
Cell Imaging ◽  
Spindle Checkpoint ◽  
Cyclin B1 ◽  
Mutant Form ◽  
Exact Time ◽  
Sister Chromatids ◽  
Sister Chromatid Separation

Progress through mitosis is controlled by the sequential destruction of key regulators including the mitotic cyclins and securin, an inhibitor of anaphase whose destruction is required for sister chromatid separation. Here we have used live cell imaging to determine the exact time when human securin is degraded in mitosis. We show that the timing of securin destruction is set by the spindle checkpoint; securin destruction begins at metaphase once the checkpoint is satisfied. Furthermore, reimposing the checkpoint rapidly inactivates securin destruction. Thus, securin and cyclin B1 destruction have very similar properties. Moreover, we find that both cyclin B1 and securin have to be degraded before sister chromatids can separate. A mutant form of securin that lacks its destruction box (D-box) is still degraded in mitosis, but now this is in anaphase. This destruction requires a KEN box in the NH2 terminus of securin and may indicate the time in mitosis when ubiquitination switches from APCCdc20 to APCCdh1. Lastly, a D-box mutant of securin that cannot be degraded in metaphase inhibits sister chromatid separation, generating a cut phenotype where one cell can inherit both copies of the genome. Thus, defects in securin destruction alter chromosome segregation and may be relevant to the development of aneuploidy in cancer.

scholarly journals Chiasmata and the kinetochore component Dam1 are crucial for elimination of erroneous chromosome attachments and centromere oscillation at meiosis I

Open Biology ◽  
2021 ◽  
Vol 11 (2) ◽  
Author(s):  
Misuzu Wakiya ◽  
Eriko Nishi ◽  
Shinnosuke Kawai ◽  
Kohei Yamada ◽  
Kazuhiro Katsumata ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Spindle Pole ◽  
Oriented Attachment ◽  
Aurora B ◽  
Correction Factors ◽  
Homologous Chromosomes ◽  
Spindle Poles ◽  
Sister Chromatids ◽  
Potential Link ◽  
Meiosis I

Establishment of proper chromosome attachments to the spindle requires elimination of erroneous attachments, but the mechanism of this process is not fully understood. During meiosis I, sister chromatids attach to the same spindle pole (mono-oriented attachment), whereas homologous chromosomes attach to opposite poles (bi-oriented attachment), resulting in homologous chromosome segregation. Here, we show that chiasmata that link homologous chromosomes and kinetochore component Dam1 are crucial for elimination of erroneous attachments and oscillation of centromeres between the spindle poles at meiosis I in fission yeast. In chiasma-forming cells, Mad2 and Aurora B kinase, which provides time for attachment correction and destabilizes erroneous attachments, respectively, caused elimination of bi-oriented attachments of sister chromatids, whereas in chiasma-lacking cells, they caused elimination of mono-oriented attachments. In chiasma-forming cells, in addition, homologous centromere oscillation was coordinated. Furthermore, Dam1 contributed to attachment elimination in both chiasma-forming and chiasma-lacking cells, and drove centromere oscillation. These results demonstrate that chiasmata alter attachment correction patterns by enabling error correction factors to eliminate bi-oriented attachment of sister chromatids, and suggest that Dam1 induces elimination of erroneous attachments. The coincidental contribution of chiasmata and Dam1 to centromere oscillation also suggests a potential link between centromere oscillation and attachment elimination.

scholarly journals Cyclin B3 promotes APC/C activation and anaphase I onset in oocyte meiosis

2018 ◽  
Author(s):  
Mehmet E. Karasu ◽  
Nora Bouftas ◽  
Scott Keeney ◽  
Katja Wassmann
Keyword(s):  
Chromosome Segregation ◽  
Mammalian Cells ◽  
Cyclin B1 ◽  
Biochemical Properties ◽  
Cellular Functions ◽  
Meiotic Progression ◽  
Oocyte Meiosis ◽  
Sterile Mutant ◽  
Essential Function ◽  
Cyclin B3

As obligate kinase partners, cyclins control the switch-like cell cycle transitions that orchestrate orderly duplication and segregation of genomes. Meiosis, the cell division that generates gametes for sexual reproduction, poses unique challenges because two rounds of chromosome segregation must be executed without intervening DNA replication. Mammalian cells express numerous, temporally regulated cyclins, but how these proteins collaborate to control meiosis remains poorly understood. Here, we delineate an essential function for mouse cyclin B3 in the first meiotic division of oocytes. Females genetically ablated for cyclin B3 are viable, indicating the protein is dispensable for mitotic divisions, but are sterile. Mutant oocytes appear normal until metaphase I but then display a highly penetrant failure to transition to anaphase I. They arrest with hallmarks of defective APC/C activation, including no separase activity and high MPF, cyclin B1, and securin levels. Partial APC/C activation occurs, however, as exogenously expressed APC/C substrates can be degraded and arrest can be suppressed by inhibiting MPF kinase. Cyclin B3 is itself targeted for degradation by the APC/C. Cyclin B3 forms active kinase complexes with CDK1, and meiotic progression requires cyclin B3-associated kinase activity. Collectively, our findings indicate that cyclin B3 is essential for oocyte meiosis because it fine-tunes APC/C activity as a kinase-activating CDK partner. Cyclin B3 homologs from frog, zebrafish, and fruitfly rescue meiotic progression in cyclin B3-deficient mouse oocytes, indicating conservation of the biochemical properties and possibly cellular functions of this germline-critical cyclin.

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
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