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Bub1 is not required for the checkpoint response to unattached kinetochores in diploid human cells

Cerys E. Currie, Mar Mora-Santos, Chris Smith, View ORCID ProfileAndrew D. McAinsh, View ORCID ProfileJonathan B.A. Millar
doi: https://doi.org/10.1101/278820
Cerys E. Currie
1Centre for Mechanochemical Cell Biology & Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Gibbet Hill, Coventry, CV4 7AL, UK
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Mar Mora-Santos
1Centre for Mechanochemical Cell Biology & Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Gibbet Hill, Coventry, CV4 7AL, UK
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Chris Smith
1Centre for Mechanochemical Cell Biology & Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Gibbet Hill, Coventry, CV4 7AL, UK
2Present address: Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Institute of Metabolic Science, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 0QQ, UK
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Andrew D. McAinsh
1Centre for Mechanochemical Cell Biology & Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Gibbet Hill, Coventry, CV4 7AL, UK
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  • For correspondence: J.Millar@warwick.ac.uk a.d.mcainsh@warwick.ac.uk
Jonathan B.A. Millar
1Centre for Mechanochemical Cell Biology & Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Gibbet Hill, Coventry, CV4 7AL, UK
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  • ORCID record for Jonathan B.A. Millar
  • For correspondence: J.Millar@warwick.ac.uk a.d.mcainsh@warwick.ac.uk
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Abstract

Error-free chromosome segregation during mitosis depends on a functional spindle assembly checkpoint (SAC). The SAC is a multi-component signaling system that is recruited to incorrectly attached kinetochores to catalyze the formation of a soluble inhibitor, known as the mitotic checkpoint complex (MCC), which binds and inhibits the anaphase promoting complex [1]. We have previously proposed that two separable pathways, composed of KNL1-Bub3-Bub1 (KBB) and Rod-Zwilch-Zw10 (RZZ), recruit Mad1-Mad2 complexes to human kinetochores to activate the SAC [2]. We refer to this as the dual pathway model. Although Bub1 is absolutely required for MCC formation in yeast (which lack RZZ), there is conflicting evidence as to whether this is also the case in human cells based on siRNA studies [2–5]. Here we report, using genome editing, that Bub1 is not strictly required for the SAC response to unattached kinetochores in human diploid hTERT-RPE1 cells, consistent with the dual pathway model.

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Posted March 08, 2018.
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Bub1 is not required for the checkpoint response to unattached kinetochores in diploid human cells
Cerys E. Currie, Mar Mora-Santos, Chris Smith, Andrew D. McAinsh, Jonathan B.A. Millar
bioRxiv 278820; doi: https://doi.org/10.1101/278820
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Bub1 is not required for the checkpoint response to unattached kinetochores in diploid human cells
Cerys E. Currie, Mar Mora-Santos, Chris Smith, Andrew D. McAinsh, Jonathan B.A. Millar
bioRxiv 278820; doi: https://doi.org/10.1101/278820

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