The dynamics of cyclin B1 distribution during meiosis I in mouse oocytes

Marangos, Petros; Carroll, John

doi:10.1530/rep.1.00192

Cited by 64 publications

(50 citation statements)

References 63 publications

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“…Another possible explanation is that the spindle is required for efficient APC/C-mediated substrate degradation. In support of this notion, the proteasome localises to the spindle apparatus in rat oocytes (Josefsberg et al 2000) and Cdc20, cyclin B and securin have all been shown to localise to the spindle in mouse oocytes (Marangos & Carroll 2004, Tsurumi et al 2004. Furthermore, artificial induction of intracellular calcium transients by ionophores, efficiently triggered homologue disjunction in metaphase I-arrested oocytes but only if an intact spindle was present (Soewarto et al 1995).…”

Section: Characterising the Meiosis I Arrest Induced By Spindle Depolmentioning

confidence: 89%

“…3D and G), indicating that differences in GFP profiles represented true differences in turnover of GFP-tagged chimerae and were not due to artefacts in the imaging technique. Secondly, high levels of securin or cyclin B could potentially saturate the destruction machinery thereby inhibiting protein degradation and meiosis I (Ledan et al 2001, Herbert et al 2003, Terret et al 2003, Marangos & Carroll 2004). This was not the reason for meiosis I arrest in nocodazoletreated oocytes however as, compared with controls, drug-exposed oocytes translated either similar (Fig.…”

Section: Spindle Depolymerisation Stabilises Securin and Cyclin B Formentioning

confidence: 99%

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Mad2 is required for inhibiting securin and cyclin B degradation following spindle depolymerisation in meiosis I mouse oocytes

Homer¹,

McDougall²,

Levasseur³

et al. 2005

Reproduction

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Mad2 is a pivotal component of the spindle assembly checkpoint (SAC) which inhibits anaphase promoting complex/cyclosome (APC/C) activity by sequestering Cdc20 thereby regulating the destruction of securin and cyclin B. During mitosis, spindle depolymerisation induces a robust Mad2-dependent arrest due to inhibition of securin and cyclin B destruction. In contrast to mitosis, the molecular details underpinning the meiosis I arrest experienced by mouse oocytes exposed to spindle depolymerisation remain incompletely characterised. Notably, the role of Mad2 and the fate of the anaphase-marker, securin, are unexplored. As shown previously, we find that spindle depolymerisation by nocodazole inhibits first polar body extrusion (PBE) and stabilises cyclin B and cyclin-dependent kinase 1 activity in mouse oocytes. Here we show that stabilisation of cyclin B in nocodazole can be sustained for several hours and is associated with stabilisation of securin. These effects are SAC-mediated as, in oocytes depleted of the majority of Mad2 by morpholino antisense, securin and cyclin B are destabilised and 15% of oocytes undergo PBE. This reflects premature APC/C activation as a mutant form of cyclin B lacking its APC/C degradation signal is stable in Mad2-depleted oocytes. Moreover, homologues do not disjoin during the prolonged meiosis I arrest (>18 h) induced by nocodaozole indicating that a non-cleavage mechanism is insufficient on its own for resolution of arm cohesion in mammalian oocytes. In conclusion, when all kinetochores lack attachment and tension, mouse oocytes mount a robust Mad2-dependent meiosis I arrest which inhibits the destruction of securin and cyclin B.

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Section: Characterising the Meiosis I Arrest Induced By Spindle Depolmentioning

confidence: 89%

Section: Spindle Depolymerisation Stabilises Securin and Cyclin B Formentioning

confidence: 99%

Mad2 is required for inhibiting securin and cyclin B degradation following spindle depolymerisation in meiosis I mouse oocytes

Homer¹,

McDougall²,

Levasseur³

et al. 2005

Reproduction

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show abstract

“…It enters the germinal vesicle just prior to GVBD (Marangos & Carroll 2004). After GVBD, the level of synthesis of cyclin B increases progressively, reaching its maximum at the end of the first meiotic M phase, and the newly synthesized protein becomes associated immediately with the p34 cdk1 kinase to form an active complex (Hampl & Eppig 1995, Winston 1997, Ledan et al 2001.…”

Section: Cyclin B Metabolism Controls the Timing Of Meiotic Maturationmentioning

confidence: 99%

Cytoskeleton and cell cycle control during meiotic maturation of the mouse oocyte: integrating time and space

Brunet

Maro²

2005

Reproduction

199

169

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During meiotic maturation of mammalian oocytes, two successive divisions occur without an intermediate phase of DNA replication, so that haploid gametes are produced. Moreover, these two divisions are asymmetric, to ensure that most of the maternal stores are retained within the oocyte. This leads to the formation of daughter cells with different sizes: the large oocyte and the small polar bodies. All these events are dependent upon the dynamic changes in the organization of the oocyte cytoskeleton (microtubules and microfilaments) and are highly regulated in time and space. We review here the current knowledge of the interplay between the cytoskeleton and the cell cycle machinery in mouse oocytes, with an emphasis on the two major activities that control meiotic maturation in vertebrates, MPF (Maturation promoting factor) and CSF (Cytostatic factor).

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“…Then, cyclin B1 forms a complex with CDK1 and the newly formed cyclin B1-CDK1 complexes are activated (15,16). Once DNA is damaged, cyclin B-CDK1 complexes are inactivated and the cells are blocked in G2 phase (17).…”

Section: Discussionmentioning

confidence: 99%

Hepatitis B virus X protein (HBx) induces G2/M arrest and apoptosis through sustained activation of cyclin B1-CDK1 kinase

Cheng¹,

Li²,

Yang³

et al. 2009

Oncol Rep

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Abstract. Hepatitis B virus X protein (HBx) is a multifunctional regulatory protein that is known to be involved in viral proliferation, transcriptional activation and cell growth control. However, the actual role of HBx in cell growth control remains controversial. In this study, the impact of HBx on cell growth in vitro and in vivo was further investigated. HBx was able to inhibit the growth of hepatocellular carcinoma (HCC) cells and induce G2/M arrest in vitro. Moreover, unlike many other G2/M arrest mechanisms, HBx did not inhibit cyclin B1-CDK1 kinase activity, but it persistently activated the cyclin B1-CDK1 kinase. In vivo, HBx inhibited tumor cell growth and induced apoptosis as well as inhibited the growth of vascular endothelial cells. In conclusion, HBx induced G2/M arrest and apoptosis through sustained activation of cyclin B1-CDK1 kinase, and negatively regulated cell growth in vitro and in vivo.

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The dynamics of cyclin B1 distribution during meiosis I in mouse oocytes

Cited by 64 publications

References 63 publications

Mad2 is required for inhibiting securin and cyclin B degradation following spindle depolymerisation in meiosis I mouse oocytes

Mad2 is required for inhibiting securin and cyclin B degradation following spindle depolymerisation in meiosis I mouse oocytes

Cytoskeleton and cell cycle control during meiotic maturation of the mouse oocyte: integrating time and space

Hepatitis B virus X protein (HBx) induces G2/M arrest and apoptosis through sustained activation of cyclin B1-CDK1 kinase

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