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. 2020 May 25;15:9. doi: 10.1186/s13008-020-00065-2

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — The three transitions of the mitotic cycle involving Cdk1-Cyclin B. During the G2-phase, Cyclin B accumulates and binds to Cdk1 that is phosphorylated at T161 by CAK and at Y15 and T14 by Wee1/Myt1. The complex is thus inactive. At the G2-to-M transition, Wee1/Myt1 are turned off while Cdc25 is turned on, promoting Y15 and T14 dephosphorylations and Cdk1 activation. During M-phase, Cdk1-Cyclin B phosphorylates many mitotic substrates, including Wee1/Myt1 and Cdc25. At the end of M-phase, MPF activates the Cyclin proteolytic degradation system, thus inducing its own inactivation