NCBI Summary:
Cyclin B2 is a member of the cyclin family, specifically the B-type cyclins. The B-type cyclins, B1 and B2, associate with p34cdc2 and are essential components of the cell cycle regulatory machinery. B1 and B2 differ in their subcellular localization. Cyclin B1 co-localizes with microtubules, whereas cyclin B2 is primarily associated with the Golgi region. Cyclin B2 also binds to transforming growth factor beta RII and thus cyclin B2/cdc2 may play a key role in transforming growth factor beta-mediated cell cycle control. [provided by RefSeq, Jul 2008]
General function
Cytoskeleton, Microtubule binding, Enzyme
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Cellular localization
Cytoplasmic, Other Membrane, Nuclear
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Ovarian function
Oogenesis, Oocyte maturation
Comment
The Translation of Cyclin B1 and B2 is Differentially Regulated during Mouse Oocyte Reentry into the Meiotic Cell Cycle. Han SJ et al. (2017) Control of protein turnover is critical for meiotic progression. Using RiboTag immunoprecipitation, RNA binding protein immunoprecipitation, and luciferase reporter assay, we investigated how rates of mRNA translation, protein synthesis and degradation contribute to the steady state level of Cyclin B1 and B2 in mouse oocytes. Ribosome loading onto Ccnb1 and Mos mRNAs increases during cell cycle reentry, well after germinal vesicle breakdown (GVBD). This is followed by the translation of reporters containing 3' untranslated region of Mos or Ccnb1 and the accumulation of Mos and Cyclin B1 proteins. Conversely, ribosome loading onto Ccnb2 mRNA and Cyclin B2 protein level undergo minimal changes during meiotic reentry. Degradation rates of Cyclin B1 or B2 protein at the GV stage are comparable. The translational activation of Mos and Ccnb1, but not Ccnb2, mRNAs is dependent on the RNA binding protein CPEB1. Inhibition of Cdk1 activity, but not Aurora A kinase activity, prevents the translation of Mos or Ccnb1 reporters, suggesting that MPF is required for their translation in mouse oocytes. Conversely, Ccnb2 translation is insensitive to Cdk1 inhibition. Thus, the poised state that allows rapid meiotic reentry in mouse GV oocytes may be determined by the differential translational control of two Cyclins.//////////////////
Analysis of the Roles of Cyclin B1 and Cyclin B2 in Porcine Oocyte Maturation by Inhibiting Synthesis with Antisense RNA Injection
Kuroda T, et al 2004 .
The function of cyclin B1 (CB1) and cyclin B2 (CB2) during porcine oocyte maturation was investigated by injecting oocytes with their antisense RNAs (asRNAs). At first, protein levels of both cyclin Bs were examined by immunoblotting, revealing that immature oocytes had only CB2, at a level comparable to 1/20 to 1/40 of that detected in first metaphase oocytes. Both cyclin B syntheses were started around germinal vesicle breakdown (GVBD); CB1 and CB2 peaked at the second metaphase and first metaphase, respectively. We obtained a porcine CB2 cDNA fragment, which was 88% homologous with human CB2, by RT-PCR using total RNAs of immature porcine oocytes and a primer set of human CB2. Specific asRNAs of CB1 and CB2 were prepared in vitro. Then one or the other or both was injected into the cytoplasm of immature oocytes. CB1 asRNA inhibited CB1 synthesis specifically; the injected oocytes underwent first meiosis normally but could not arrest at the second meiotic metaphase. CB2 asRNA inhibited CB2 synthesis specifically, but had almost no effect on the maturation of injected oocytes. When both CB1 and CB2 asRNAs were injected, synthesis of both cyclin Bs was inhibited and GVBD was significantly suppressed but occurred slowly. These results suggest that CB1 is the principal molecule for regulation in mammalian oocyte maturation, whereas CB2 has only accessory role. They also show that, in porcine oocytes, cyclin B synthesis is not necessary for GVBD induction itself, but synthesis of at least one cyclin B, CB1 or CB2, is necessary for GVBD induction in a normal time-course.
The influence of follicle size, FSH-enriched maturation medium, and early cleavage on bovine oocyte maternal mRNA levels. Mourot M et al. Transcription is arrested in the bovine oocyte within the first few hours of in vitro maturation, thus the stored maternal mRNAs accumulated in the oocyte are essential to sustain development until the Maternal-Zygotic Transition. In vivo matured oocytes have superior blastocyst formation rates than in vitro matured oocytes, suggesting that the mRNA content of these oocytes is of higher quality. To determine which transcripts may be associated with developmental competence, a Suppressive Subtractive Hybridization was performed between oocytes collected by ovariectomy at 6 hr post-LH surge and oocytes from slaughterhouse collected after 6 hr of maturation, resulting in a library enriched in these functionally important mRNAs. The clones were spotted onto a cDNA microarray and transcripts potentially associated with developmental competence were hybridized onto these slides. Hybridizations were performed with transcripts up-regulated in oocytes cultured for 6 hr in the presence or absence of rFSH in vitro, and secondly with transcripts up regulated in early-cleaving embryos versus those at the one-cell stage at 36 hr postfertilization. From these hybridizations, 13 candidates were selected. Their functional association with embryonic competence was validated by measuring their relative transcript levels by quantitative real-time PCR in eight different conditions: oocytes cultured with or without rFSH, early-versus late-cleaving embryos, and oocytes from different follicle sizes (1-3, 3-5, 5-8, and >8 mm of diameter). The gene candidates CCNB2, PTTG1, H2A, CKS1, PSMB2, SKIIP, CDC5L, RGS16, and PRDX1 showed a significant quantitative association with competence compared to BMP15, GDF9, CCNB1, and STK6. Mol. Reprod. Dev. (c) 2006 Wiley-Liss, Inc.
Expression regulated by
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Ovarian localization
Oocyte
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Hec1-Dependent Cyclin B2 Stabilization Regulates the G2-M Transition and Early Prometaphase in Mouse Oocytes. Gui L et al. The functions of the Ndc80/Hec1 subunit of the highly conserved Ndc80 kinetochore complex are normally restricted to M phase when it exerts a pivotal kinetochore-based role. Here, we find that in mouse oocytes, depletion of Hec1 severely compromises the G2-M transition because of impaired activation of cyclin-dependent kinase 1 (Cdk1). Unexpectedly, impaired M phase entry is due to instability of the Cdk1-activating subunit, cyclin B2, which cannot be covered by cyclin B1. Hec1 protects cyclin B2 from destruction by the Cdh1-activated anaphase-promoting complex (APC(Cdh1)) and remains important for cyclin B2 stabilization during early M phase, required for the initial stages of acentrosomal spindle assembly. By late M phase, however, Hec1 and cyclin B2 become uncoupled, and although Hec1 remains stable, APC(Cdc20) triggers cyclin B2 destruction. These data identify another dimension to Hec1 function centered on M phase entry and early prometaphase progression and challenge the view that cyclin B2 is completely dispensable in mammals.
Follicle stages
Antral, Preovulatory
Comment
Phenotypes
Mutations
2 mutations
Species: mouse
Mutation name: type: null mutation fertility: subfertile Comment: Cyclin B2 is required for progression through meiosis in mouse oocytes. Daldello EM et al. (2019) Cyclins associate with CDK1 to generate the M-phase-promoting factor (MPF) activity essential for progression through mitosis and meiosis. Although CCNB1 is required for embryo development, previous studies concluded that CCNB2 is dispensable for cell cycle progression. Given our findings of high CcnB2 mRNA translation rates in prophase-arrested oocytes, we have reevaluated the role of this cyclin during meiosis. CcnB2-/- oocytes undergo delayed germinal vesicle breakdown and show defects during metaphase to anaphase transition. This defective maturation is associated with compromised CcnB1 and Mos mRNA translation, delayed spindle assembly, and increased errors in chromosome segregation. Given these defects, a significant percentage of oocytes fail to complete meiosis I because the SAC remains active and APC function is inhibited. In vivo, CCNB2 depletion cause ovulation of immature oocytes, compromised female fecundity, and premature ovarian failure. These findings demonstrate that CCNB2 is required to assemble sufficient pre-MPF for timely meiosis reentry and progression. Although endogenous cyclins cannot compensate, overexpression of CCNB1/2 rescues the meiotic phenotypes, indicating similar molecular properties but divergent modes of regulation of these cyclins.//////////////////
Species: mouse
Mutation name: type: null mutation fertility: subfertile Comment: Cyclin B2 is required for progression through meiosis in mouse oocytes. Daldello EM et al. (2019) Cyclins associate with CDK1 to generate the M-phase-promoting factor (MPF) activity essential for progression through mitosis and meiosis. Although CCNB1 is required for embryo development, previous studies concluded that CCNB2 is dispensable for cell cycle progression. Given our findings of high CcnB2 mRNA translation rates in prophase-arrested oocytes, we have reevaluated the role of this cyclin during meiosis. CcnB2-/- oocytes undergo delayed germinal vesicle breakdown and show defects during metaphase to anaphase transition. This defective maturation is associated with compromised CcnB1 and Mos mRNA translation, delayed spindle assembly, and increased errors in chromosome segregation. Given these defects, a significant percentage of oocytes fail to complete meiosis I because the SAC remains active and APC function is inhibited. In vivo, CCNB2 depletion cause ovulation of immature oocytes, compromised female fecundity, and premature ovarian failure. These findings demonstrate that CCNB2 is required to assemble sufficient pre-MPF for timely meiosis reentry and progression. Although endogenous cyclins cannot compensate, overexpression of CCNB1/2 rescues the meiotic phenotypes, indicating similar molecular properties but divergent modes of regulation of these cyclins.//////////////////