Chromosome biorientation and APC activity remain uncoupled in oocytes with reduced volume

Lane, Simon I. R.; Jones, Kevin

doi:10.1083/jcb.201606134

Cited by 29 publications

(27 citation statements)

References 46 publications

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“…Crucially, the outcome depended upon the stage of oogenesis at which bisection was performed ( Figure 3). If oocytes were bisected just after germinal vesicle breakdown, the impact of cytoplasm reduction upon SAC was relatively minor, and misaligned chromosomes still failed to prevent anaphase even in very small mini-oocytes (13% original size) [90]. However, if the bisection occurred prior to germinal vesicle breakdown, then misaligned chromosomes more clearly arrested the cell cycle, even if oocyte volume was reduced only by half [91].…”

Section: Idiosyncratic Spindle Assembly Checkpoint In Oocyte Meiosis-imentioning

confidence: 99%

“…However, if the bisection occurred prior to germinal vesicle breakdown, then misaligned chromosomes more clearly arrested the cell cycle, even if oocyte volume was reduced only by half [91]. The difference likely pertains to the observation that some SAC components assemble at the nucleus in interphase [92], such that bisection prior to germinal vesicle breakdown effectively concentrates SAC components, whereas bisection after germinal vesicle breakdown reduces cell volume without influencing SAC component concentrations [90,91]. Whether the effect of size will be more apparent in the human oocyte, which is approximately three to four times greater in volume than mouse, and whether the same principle causes the SAC to strengthen during early embryonic development, when cell divisions are also error prone and cells progressively decrease in size and nuclear-cytoplasmic ratio increases [93,94], will be interesting to determine.…”

Section: Idiosyncratic Spindle Assembly Checkpoint In Oocyte Meiosis-imentioning

confidence: 99%

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Segregating Chromosomes in the Mammalian Oocyte

Mihajlović

FitzHarris

2018

Current Biology

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Chromosome segregation errors in human oocytes lead to aneuploid embryos that cause infertility and birth defects. Here we provide an overview of the chromosome-segregation process in the mammalian oocyte, highlighting mechanistic differences between oocytes and somatic cells that render oocytes so prone to segregation error. These differences include the extremely large size of the oocyte cytoplasm, the unique geometry of meiosis-I chromosomes, idiosyncratic function of the spindle assembly checkpoint, and dramatically altered oocyte cell-cycle control and spindle assembly, as compared to typical somatic cells. We summarise recent work suggesting that aging leads to a further deterioration in fidelity of chromosome segregation by impacting multiple components of the chromosome-segregation machinery. In addition, we compare and contrast recent results from mouse and human oocytes, which exhibit overlapping defects to differing extents. We conclude that the striking propensity of the oocyte to mis-segregate chromosomes reflects the unique challenges faced by the spindle in a highly unusual cellular environment.

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Section: Idiosyncratic Spindle Assembly Checkpoint In Oocyte Meiosis-imentioning

confidence: 99%

Section: Idiosyncratic Spindle Assembly Checkpoint In Oocyte Meiosis-imentioning

confidence: 99%

Segregating Chromosomes in the Mammalian Oocyte

Mihajlović

FitzHarris

2018

Current Biology

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“…In vitro experiments using Xenopus laevis egg extracts suggested that an increased nuclear to cytoplasmic ratio, as would be found in smaller cells, could increase SAC activity ( Minshull et al , 1994 ). Recent work in Caenorhabditis elegans embryos and mouse oocytes has shown that the strength of the SAC indeed scales with cell size, with smaller cells exhibiting a stronger SAC ( Galli and Morgan, 2016 ; Kyogoku and Kitajima, 2017 ; Lane and Jones, 2017 ). However, in other organisms, the SAC remains inactive until the midblastula transition and acquisition of SAC activity is neither accelerated by decreasing cell volume ( X. laevis ; Clute and Masui, 1995 , 1997 ) nor delayed by increasing cell volume ( Danio rerio ; Zhang et al , 2015 ), indicating that SAC activity can also be developmentally regulated independently of changes in cell volume.…”

Section: Introductionmentioning

confidence: 99%

Spindle assembly checkpoint strength is linked to cell fate in theCaenorhabditis elegansembryo

Gerhold

Poupart

Labbé

et al. 2018

MBoC

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The spindle assembly checkpoint (SAC) is a conserved mitotic regulator that preserves genome stability by monitoring kinetochore–microtubule attachments and blocking anaphase onset until chromosome biorientation is achieved. Despite its central role in maintaining mitotic fidelity, the ability of the SAC to delay mitotic exit in the presence of kinetochore–microtubule attachment defects (SAC “strength”) appears to vary widely. How different cellular aspects drive this variation remains largely unknown. Here we show that SAC strength is correlated with cell fate during development of Caenorhabditis elegans embryos, with germline-fated cells experiencing longer mitotic delays upon spindle perturbation than somatic cells. These differences are entirely dependent on an intact checkpoint and only partially attributable to differences in cell size. In two-cell embryos, cell size accounts for half of the difference in SAC strength between the larger somatic AB and the smaller germline P1 blastomeres. The remaining difference requires asymmetric cytoplasmic partitioning downstream of PAR polarity proteins, suggesting that checkpoint-regulating factors are distributed asymmetrically during early germ cell divisions. Our results indicate that SAC activity is linked to cell fate and reveal a hitherto unknown interaction between asymmetric cell division and the SAC.

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“…Moreover, a large cytoplasmic volume, which is a general feature of female meiosis, is directly linked to the weakened checkpoint (Kyogoku and Kitajima, 2017;Lane and Jones, 2017).…”

Section: Discussionmentioning

confidence: 99%

Molecular and evolutionary strategies of meiotic cheating by selfish centromeres

Akera

Trimm

2018

Preprint

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Asymmetric division in female meiosis creates selective pressure favoring selfish centromeres that bias their transmission to the egg. This centromere drive can explain the paradoxical rapid evolution of both centromere DNA and centromere-binding proteins despite conserved centromere function. Here, we define a molecular pathway linking expanded centromeres to histone phosphorylation and recruitment of microtubule destabilizing factors in an intraspecific hybrid, leading to detachment of selfish centromeres from spindle microtubules that would direct them to the polar body. We also introduce a second hybrid model, exploiting centromere divergence between species, and show that winning centromeres in one hybrid become losers in the other. Our results indicate that increasing destabilizing activity is a general strategy for drive, but centromeres have evolved distinct strategies to increase that activity. Furthermore, we show that drive depends on slowing meiotic progression, suggesting that a weakened meiotic spindle checkpoint evolved as a mechanism to suppress selfish centromeres.

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Chromosome biorientation and APC activity remain uncoupled in oocytes with reduced volume

Abstract: Lane and Jones use serial bisection of mouse oocytes to analyze the influence of cytoplasmic volume on spindle assembly checkpoint function. Volume reduction promotes inhibition of APC but cannot prevent chromosome segregation errors at anaphase.

Cited by 29 publications

References 46 publications

Segregating Chromosomes in the Mammalian Oocyte

Segregating Chromosomes in the Mammalian Oocyte

Spindle assembly checkpoint strength is linked to cell fate in theCaenorhabditis elegansembryo

Molecular and evolutionary strategies of meiotic cheating by selfish centromeres

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