Cdc6 is required for meiotic spindle assembly in Xenopus oocytes

Narasimhachar, Yadushyla; Webster, Daniel R.; Gard, David L.; Coué, Martine

doi:10.4161/cc.11.3.19033

Cited by 9 publications

(8 citation statements)

References 40 publications

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“…G 2 phases. Cdc6 localizes to centrosomes during the S and G 2 phases (36,37). This work demonstrates a novel function for Cdc6 at S and G 2 phase centrosomes: that Cdc6, with its ATPase activity, negatively controls both microtubule nucleation for MTOC activity and the levels of PCM proteins (Fig.…”

Section: Cdc6 Regulates Centrosome Functionmentioning

confidence: 70%

“…Cdc6 localizes to the centrosomes during the S and G 2 phases of the human cell cycle (supplemental Fig. S1, A and B) (36,37). Because the centrosome functions as a MTOC, we examined whether Cdc6 plays a role in microtubule formation.…”

Section: Cdc6 Depletion Increases Microtubule Regrowth Originating Frmentioning

confidence: 99%

“…Non-chromatin bound Cdc6 is exported from the nucleus to the cytoplasm during S phase (32,35). Furthermore, Cdc6 localizes to centrosomes during both the S and G 2 phases (36,37). In this work, we address Cdc6 function at centrosomes during the S and G 2 phases.…”

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confidence: 99%

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The DNA replication protein Cdc6 inhibits the microtubule-organizing activity of the centrosome

Lee¹,

Kim²,

Bae

et al. 2017

Journal of Biological Chemistry

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The centrosome serves as a major microtubule-organizing center (MTOC). The Cdc6 protein is a component of the pre-replicative complex and a licensing factor for the initiation of chromosome replication and localizes to centrosomes during the S and G phases of the cfell cycle of human cells. This cell cycle-dependent localization of Cdc6 to the centrosome motivated us to investigate whether Cdc6 negatively regulates MTOC activity and to determine the integral proteins that comprise the pericentriolar material (PCM). Time-lapse live-cell imaging of microtubule regrowth revealed that Cdc6 depletion increased microtubule nucleation at the centrosomes and that expression of Cdc6 in Cdc6-depleted cells reversed this effect. This increase and decrease in microtubule nucleation correlated with the centrosomal intensities of PCM proteins such as γ-tubulin, pericentrin, CDK5 regulatory subunit-associated protein 2 (CDK5RAP2), and centrosomal protein 192 (Cep192). The regulation of microtubule nucleation and the recruitment of PCM proteins to the centrosome required Cdc6 ATPase activity, as well as a centrosomal localization of Cdc6. These results suggest a novel function for Cdc6 in coordinating centrosome assembly and function.

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Section: Cdc6 Regulates Centrosome Functionmentioning

confidence: 70%

Section: Cdc6 Depletion Increases Microtubule Regrowth Originating Frmentioning

confidence: 99%

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The DNA replication protein Cdc6 inhibits the microtubule-organizing activity of the centrosome

Lee¹,

Kim²,

Bae

et al. 2017

Journal of Biological Chemistry

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“…Independently of this licensing activity, Cdc6 is required for spindle formation during mitosis and meiosis (Anger et al, 2005;Illenye and Heintz, 2004;Narasimhachar et al, 2012;Yim and Erikson, 2010). Cdc6 further regulates M-phase progression by activating checkpoint mechanisms at the G2/M transition and by inhibiting Cdk1 activity during mitosis exit (Borlado and Mendez, 2008;Erikson, 2010, 2011).…”

Section: Introductionmentioning

confidence: 99%

Fine-tuning of Cdc6 accumulation by Cdk1 and MAP kinase is essential for completion of oocyte meiotic divisions

Daldello

Poulhe

et al. 2015

Journal of Cell Science

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).In Fig. 4B, the western blot used to illustrate the elution profile of Cdk1 in the control was mistakenly used a second time to illustrate the samples incubated with anti-Cdc6 antibody. The correct Fig. 4 is shown below. This error does not affect the conclusions of the study.The authors apologise to readers for any confusion that this error might have caused. , Olivier Haccard 1,2 and Aude Dupré1 ,2, * ABSTRACT Vertebrate oocytes proceed through the first and the second meiotic division without an intervening S-phase to become haploid. Although DNA replication does not take place, unfertilized oocytes acquire the competence to replicate DNA one hour after the first meiotic division by accumulating an essential factor of the replicative machinery, Cdc6. Here, we show that the turnover of Cdc6 is precisely regulated in oocytes to avoid inhibition of Cdk1. At meiosis resumption, Cdc6 is expressed but cannot accumulate owing to a degradation mechanism that is activated through Cdk1. During transition from the first to the second meiotic division, Cdc6 is under the antagonistic regulation of B-type cyclins (which interact with and stabilize Cdc6) and the Mos-MAPK pathway (which negatively controls Cdc6 accumulation). Because overexpressing Cdc6 inhibits Cdk1 reactivation and drives oocytes into a replicative interphasic state, the fine-tuning of Cdc6 accumulation is essential to ensure two meiotic waves of Cdk1 activation and to avoid unscheduled DNA replication during meiotic maturation.

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“…Therefore, studies on the in vivo control of cell division have mainly focused on the early stages of embryogenesis when an embryo contains only a handful of cells. Such studies have successfully defined the regulatory pathways controlling cell division asynchrony or polarity (Brauchle et al , 2003 ; Colombo et al , 2003 ; Budirahardja & Gonczy, 2008 ; Galli & van den Heuvel, 2008 ; Li, 2013 ), chromosome segregation (van der Voet et al , 2009 ), cytokinesis (Sonnichsen et al , 2005 ; Chartier et al , 2011 ), and centrosome assembly (Greenan et al , 2010 ; Narasimhachar et al , 2012 ). As hundreds of cells accumulate within a developing embryo, it becomes extremely difficult to systematically document the cellular and molecular events through direct observation.…”

Section: Introductionmentioning

confidence: 99%

Systems‐level quantification of division timing reveals a common genetic architecture controlling asynchrony and fate asymmetry

Wong

et al. 2015

Molecular Systems Biology

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Coordination of cell division timing is crucial for proper cell fate specification and tissue growth. However, the differential regulation of cell division timing across or within cell types during metazoan development remains poorly understood. To elucidate the systems-level genetic architecture coordinating division timing, we performed a high-content screening for genes whose depletion produced a significant reduction in the asynchrony of division between sister cells (ADS) compared to that of wild-type during Caenorhabditis elegans embryogenesis. We quantified division timing using 3D time-lapse imaging followed by computer-aided lineage analysis. A total of 822 genes were selected for perturbation based on their conservation and known roles in development. Surprisingly, we find that cell fate determinants are not only essential for establishing fate asymmetry, but also are imperative for setting the ADS regardless of cellular context, indicating a common genetic architecture used by both cellular processes. The fate determinants demonstrate either coupled or separate regulation between the two processes. The temporal coordination appears to facilitate cell migration during fate specification or tissue growth. Our quantitative dataset with cellular resolution provides a resource for future analyses of the genetic control of spatial and temporal coordination during metazoan development.

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Cdc6 is required for meiotic spindle assembly in Xenopus oocytes

Cited by 9 publications

References 40 publications

The DNA replication protein Cdc6 inhibits the microtubule-organizing activity of the centrosome

The DNA replication protein Cdc6 inhibits the microtubule-organizing activity of the centrosome

Fine-tuning of Cdc6 accumulation by Cdk1 and MAP kinase is essential for completion of oocyte meiotic divisions

Systems‐level quantification of division timing reveals a common genetic architecture controlling asynchrony and fate asymmetry

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