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Mechanism of spindle pole organization and instability in human oocytes

MPG-Autoren
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So,  C.
Department of Meiosis, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Menelaou,  K.
Department of Meiosis, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Uraji,  J.
Department of Meiosis, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Harasimov,  K.
Department of Meiosis, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Steyer,  A. M.
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

Bucevičius,  J.
Laboratory of Chromatin Labeling and Imaging, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

Lukinavicius,  G.
Laboratory of Chromatin Labeling and Imaging, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Möbius,  W.
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Schuh,  M.
Department of Meiosis, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Zitation

So, C., Menelaou, K., Uraji, J., Harasimov, K., Steyer, A. M., Seres, K. B., et al. (2022). Mechanism of spindle pole organization and instability in human oocytes. Science, 375(6581): eabj3944. doi:10.1126/science.abj3944.


Zitierlink: https://hdl.handle.net/21.11116/0000-000A-6C08-5
Zusammenfassung
Human oocytes are prone to assembling meiotic spindles with unstable poles, which can favor aneuploidy in human eggs. The underlying causes of spindle instability are unknown. We found that NUMA (nuclear mitotic apparatus protein)–mediated clustering of microtubule minus ends focused the spindle poles in human, bovine, and porcine oocytes and in mouse oocytes depleted of acentriolar microtubule-organizing centers (aMTOCs). However, unlike human oocytes, bovine, porcine, and aMTOC-free mouse oocytes have stable spindles. We identified the molecular motor KIFC1 (kinesin superfamily protein C1) as a spindle-stabilizing protein that is deficient in human oocytes. Depletion of KIFC1 recapitulated spindle instability in bovine and aMTOC-free mouse oocytes, and the introduction of exogenous KIFC1 rescued spindle instability in human oocytes. Thus, the deficiency of KIFC1 contributes to spindle instability in human oocytes.