The spindle assembly checkpoint is not essential for CSF arrest of mouse oocytes

Tsurumi, Chizuko; Hoffmann, Steffen; Geley, Stephan; Graeser, Ralph; Polanski, Zbigniew

doi:10.1083/jcb.200405165

Cited by 140 publications

(164 citation statements)

References 48 publications

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“…We initially examined the spatial localization of chromatids in cytostatic factor (CSF)-induced metaphase II-arrested mouse oocytes 9 . Wild type and Sycp3 À / À MII oocytes were stained with Hoechst 33342 nuclear dye and analysed using cellular imaging microscopy.…”

Section: Resultsmentioning

confidence: 99%

Merotelic attachments allow alignment and stabilization of chromatids in meiosis II oocytes

2014

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The chromosome segregation process in human oocytes is highly error-prone, generating meiosis II (MII) oocytes with unbalanced chromatids that contribute to aneuploidy in offspring. This raises questions regarding the mechanism for transmission of chromatids and how chromatids evade the error correction mechanisms in MII oocytes. Here, we analyse the behaviour of chromatids in mouse MII oocytes. We find that chromatids align at the spindle equator at the metaphase stage of MII and that their presence does not obstruct entry into the anaphase stage. The alignment process is mediated by merotelic (bi-directional) microtubule-kinetochore attachments, revealing a multi-domain organization of the kinetochore of mammalian meiotic chromosomes. Our results suggest that biorientation of chromatids stabilize microtubule attachments at the kinetochores in a tension-dependent manner. Our results also suggest that merotelic attachments contribute to chromosome mis-segregation in wild-type MII oocytes. Thus, merotely is an important promoter of aneuploidy in mammalian oocytes.

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Section: Resultsmentioning

confidence: 99%

Merotelic attachments allow alignment and stabilization of chromatids in meiosis II oocytes

2014

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“…Therefore, Mos is necessary to maintain, but not establish, meiotic arrest in mouse. In addition, p90 RSK and spindle assembly checkpoint proteins are not necessary for CSF arrest in mouse, because oocytes without functional versions of these proteins arrest normally at metaphase of meiosis II (Tsurumi et al, 2004;Dumont et al, 2005).…”

Section: Meiosis Arrest and Release In Vertebratesmentioning

confidence: 99%

Transitioning from egg to embryo: Triggers and mechanisms of egg activation

Horner

Wolfner

2008

Developmental Dynamics

181

177

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The transition from mature oocyte to developing embryo requires a coordinated series of events, collectively known as egg activation. Egg activation includes changes to egg coverings to prevent polyspermy, release of oocyte meiotic arrest, generation of haploid female and male pronuclei, changes in maternal mRNAs and protein populations, and cytoskeletal rearrangements. In many animals, egg activation is triggered by fertilization, which increases intracellular calcium within the oocyte and thereby regulates molecular events of egg activation. In other animals, fertilization-independent external signals, including mechanical stimulation of eggs and/or changes in ionic milieu, trigger activation. Recent studies have clarified the upstream portion of pathways leading to eggshell changes and cell cycle resumption and have identified activation-induced changes in maternal mRNA and protein profiles that can identify molecular players in the downstream events of egg activation. We review signals that trigger activation and how they link to subsequent molecular events of egg activation. Developmental Dynamics 237:527-544, 2008.

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“…On the face of it, it is perplexing that all of the components critical for operation of this loop could potentially be present in MI, yet this feedback pathway does not appear to operate at this cell cycle stage. This is most likely due to the fact that the spindle checkpoint is operative in MI (Wassmann et al, 2003), but not during MII arrest (Tsurumi et al, 2004). This checkpoint results in profound APC inhibition until the metaphase I plate is formed, allowing constitutively high Cdc2 kinase activity and consequently rapid Emi2 turnover.…”

Section: Differential Control Of the Apc In MI And Miimentioning

confidence: 99%

Cdc2 and Mos Regulate Emi2 Stability to Promote the Meiosis I–Meiosis II Transition

Tang

Guo

et al. 2008

MBoC

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The transition of oocytes from meiosis I (MI) to meiosis II (MII) requires partial cyclin B degradation to allow MI exit without S phase entry. Rapid reaccumulation of cyclin B allows direct progression into MII, producing a cytostatic factor (CSF)-arrested egg. It has been reported that dampened translation of the anaphase-promoting complex (APC) inhibitor Emi2 at MI allows partial APC activation and MI exit. We have detected active Emi2 translation at MI and show that Emi2 levels in MI are mainly controlled by regulated degradation. Emi2 degradation in MI depends not on Ca2+/calmodulin-dependent protein kinase II (CaMKII), but on Cdc2-mediated phosphorylation of multiple sites within Emi2. As in MII, this phosphorylation is antagonized by Mos-mediated recruitment of PP2A to Emi2. Higher Cdc2 kinase activity in MI than MII allows sufficient Emi2 phosphorylation to destabilize Emi2 in MI. At MI anaphase, APC-mediated degradation of cyclin B decreases Cdc2 activity, enabling Cdc2-mediated Emi2 phosphorylation to be successfully antagonized by Mos-mediated PP2A recruitment. These data suggest a model of APC autoinhibition mediated by stabilization of Emi2; Emi2 proteins accumulate at MI exit and inhibit APC activity sufficiently to prevent complete degradation of cyclin B, allowing MI exit while preventing interphase before MII entry.

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The spindle assembly checkpoint is not essential for CSF arrest of mouse oocytes

Cited by 140 publications

References 48 publications

Merotelic attachments allow alignment and stabilization of chromatids in meiosis II oocytes

Merotelic attachments allow alignment and stabilization of chromatids in meiosis II oocytes

Transitioning from egg to embryo: Triggers and mechanisms of egg activation

Cdc2 and Mos Regulate Emi2 Stability to Promote the Meiosis I–Meiosis II Transition

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