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. 2020 Jun 23;6:42. doi: 10.1038/s41421-020-0170-2

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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. 6 — Haspin-dependent isotropic fusion of Ras-containing-vesicles on the PM is essential for a successful mitosis. During M-phase, Cdc24 relies on GTP-Ras to be recruited to the PM, possibly through direct physical interaction. This relocalization of Cdc24 promotes an even distribution of Cdc42 activity and hence polarisome dispersal. In early mitosis, the fusion of vesicles that mediate Ras-GTP delivery to the PM occurs mainly at the bud tip, causing accumulation of Cdc24 and subsequently of GTP-Cdc42 to the same region. As the cell cycle progresses through late mitosis, wt cells direct homogeneous vesicle fusion to the whole PM causing a delocalization of GTP-Ras, Cdc24, and active Cdc42 from the bud tip. Loss of haspin impairs this shift in vesicle fusion, causing a persistent polarized traffic towards the bud tip with consequent persistency of the polarity factors. This persistent polarization, in case of mitotic delays, ultimately results in defective nuclear segregation and consequent cell death.