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. 2020 May 27;11:2652. doi: 10.1038/s41467-020-16488-y

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — Different modes of spindle bipolarization. In mouse MI oocytes, Prc1 (orange) is highly enriched at kinetochores (magenta). The Prc1-rich kinetochore microenvironment is required for driving slow bipolarization of the spindle (green). This kinetochore-dependent spindle bipolarization is critical for MI to prevent chromosome segregation errors. In mouse MII oocytes, the cytoplasmic environment that contains upregulated factors including Prc1 provides global support to rapid, kinetochore-independent pathways for spindle bipolarization. In human MI oocytes, spindle bipolarization occurs without kinetochore-enriched Prc1, and is error prone.