scholarly journals G2/Mitotic-Specific Cyclin-B3

2020 ◽  
Author(s):  
Keyword(s):  
Cell Cycle ◽  
2015 ◽  
Vol 14 (16) ◽  
pp. 2648-2654 ◽  
Author(s):  
Teng Zhang ◽  
Shu-Tao Qi ◽  
Lin Huang ◽  
Xue-Shan Ma ◽  
Ying-Chun Ouyang ◽  
...  

2018 ◽  
Vol 28 (7) ◽  
pp. 1150-1156.e4 ◽  
Author(s):  
Nicholas Treen ◽  
Tyler Heist ◽  
Wei Wang ◽  
Michael Levine

2002 ◽  
Vol 291 (2) ◽  
pp. 406-413 ◽  
Author(s):  
Jean-Claude Lozano ◽  
Eric Perret ◽  
Philippe Schatt ◽  
Cécile Arnould ◽  
Gérard Peaucellier ◽  
...  

2019 ◽  
Vol 218 (4) ◽  
pp. 1265-1281 ◽  
Author(s):  
Mehmet E. Karasu ◽  
Nora Bouftas ◽  
Scott Keeney ◽  
Katja Wassmann

Meiosis 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 show that female mice genetically ablated for cyclin B3 are viable—indicating that 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 anaphase-promoting complex/cyclosome (APC/C) activation, including no separase activity, high CDK1 activity, and high cyclin B1 and securin levels. Partial APC/C activation occurs, however, as exogenously expressed APC/C substrates can be degraded. Cyclin B3 forms active kinase complexes with CDK1, and meiotic progression requires cyclin B3–associated kinase activity. Cyclin B3 homologues from frog, zebrafish, and fruit fly rescue meiotic progression in cyclin B3–deficient mouse oocytes, indicating conservation of the biochemical properties and possibly cellular functions of this germline-critical cyclin.


2018 ◽  
Vol 28 (8) ◽  
pp. 1330-1331 ◽  
Author(s):  
Nicholas Treen ◽  
Tyler Heist ◽  
Wei Wang ◽  
Michael Levine

2015 ◽  
Vol 25 (6) ◽  
pp. 811-816 ◽  
Author(s):  
Kai Yuan ◽  
Patrick H. O’Farrell
Keyword(s):  

2020 ◽  
Author(s):  
Damien Garrido ◽  
Mohammed Bourouh ◽  
Éric Bonneil ◽  
Pierre Thibault ◽  
Andrew Swan ◽  
...  

ABSTRACTIn mitosis and meiosis, chromosome segregation is triggered by the Anaphase-Promoting Complex/Cyclosome (APC/C), a multi-subunit ubiquitin ligase that targets proteins for degradation, leading to the separation of chromatids. APC/C activation requires phosphorylation of its APC3 and APC1 subunits, which allows the APC/C to bind its Cdc20 co-activator. The identity of the kinase(s) responsible for APC/C activation in vivo is unclear. Cyclin B3 is required for meiotic anaphase in flies, worms and vertebrates, but whether it activates the APC/C is unclear. We found that Drosophila Cyclin B3 (CycB3) collaborates with PP2A-B55/Tws in embryonic development, indicating that CycB3 also promotes anaphase in mitosis. Moreover, CycB3 promotes APC/C activity and anaphase in cells in culture. We show that CycB3 physically associates with the APC/C, is required for phosphorylation of APC3, and promotes APC/C association with its co-activators. We propose that CycB3-Cdk1 directly phosphorylates the APC/C to activate it in both meiosis and mitosis.


2018 ◽  
Author(s):  
Mehmet E. Karasu ◽  
Nora Bouftas ◽  
Scott Keeney ◽  
Katja Wassmann

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.


2019 ◽  
Author(s):  
Mehmet E. Karasu ◽  
Scott Keeney

AbstractCyclins, as regulatory partners of cyclin-dependent kinases (CDKs), control the switch-like cell cycle transitions that orchestrate orderly duplication and segregation of genomes. Compared to mitosis, relatively little is known about how cyclin-CDK complexes control meiosis, the specialized cell division that generates gametes for sexual production. Mouse cyclin B3 was previously shown to have expression restricted to the beginning of meiosis, making it a candidate to regulate meiotic events. Indeed, female mice lacking cyclin B3 are sterile because oocytes arrest at the metaphase-to-anaphase transition of meiosis I. However, whether cyclin B3 functions during spermatogenesis was untested. Here, we found that males lacking cyclin B3 are fertile and show no detectable defects in spermatogenesis based on histological analysis of seminiferous tubules. Cytological analysis further showed no detectable defects in homologous chromosome synapsis or meiotic progression, and suggested that recombination is initiated and completed efficiently. Moreover, absence of cyclin B3 did not exacerbate previously described meiotic defects in mutants deficient for cyclin E2, suggesting a lack of redundancy between these cyclins. Thus, unlike in females, cyclin B3 is not essential for meiosis in males despite its prominent meiosis-specific expression.


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