Toggle Main Menu Toggle Search

Open Access padlockePrints

Prc1-rich kinetochores are required for error-free acentrosomal spindle bipolarization during meiosis I in mouse oocytes

Lookup NU author(s): Dr Lisa Ferguson, Dr Meenakshi Choudhary, Professor Mary Herbert



This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


© 2020, The Author(s).Acentrosomal meiosis in oocytes represents a gametogenic challenge, requiring spindle bipolarization without predefined bipolar cues. While much is known about the structures that promote acentrosomal microtubule nucleation, less is known about the structures that mediate spindle bipolarization in mammalian oocytes. Here, we show that in mouse oocytes, kinetochores are required for spindle bipolarization in meiosis I. This process is promoted by oocyte-specific, microtubule-independent enrichment of the antiparallel microtubule crosslinker Prc1 at kinetochores via the Ndc80 complex. In contrast, in meiosis II, cytoplasm that contains upregulated factors including Prc1 supports kinetochore-independent pathways for spindle bipolarization. The kinetochore-dependent mode of spindle bipolarization is required for meiosis I to prevent chromosome segregation errors. Human oocytes, where spindle bipolarization is reportedly error prone, exhibit no detectable kinetochore enrichment of Prc1. This study reveals an oocyte-specific function of kinetochores in acentrosomal spindle bipolarization in mice, and provides insights into the error-prone nature of human oocytes.

Publication metadata

Author(s): Yoshida S, Nishiyama S, Lister L, Hashimoto S, Mishina T, Courtois A, Kyogoku H, Abe T, Shiraishi A, Choudhary M, Nakaoka Y, Herbert M, Kitajima TS

Publication type: Article

Publication status: Published

Journal: Nature Communications

Year: 2020

Volume: 11

Issue: 1

Online publication date: 27/05/2020

Acceptance date: 01/05/2020

Date deposited: 08/06/2020

ISSN (electronic): 2041-1723

Publisher: Nature Research


DOI: 10.1038/s41467-020-16488-y

PubMed id: 32461611


Altmetrics provided by Altmetric