Spatiotemporal control of mitotic exit during anaphase by an aurora B-Cdk1 crosstalk

• Type: Article in International Scientific Journal
• Date: 2019

Authors

Afonso, O (Author) Other; Castellani, CM (Author) Other; Cheeseman, LP (Author) Other; J Ferreira (Author) FMUP; Orr, B (Author) Other; Ferreira, LT (Author) Other; Chambers, JJ (Author) Other; Morais de Sa, E (Author) Other; Maresca, TJ (Author) Other; Helder Maiato (Author) FMUP

Journal

Title: eLife

Vol. 8

ISSN: 2050-084X

Publisher: eLife Sciences Publications

Indexing

ISI Web of Knowledge - 23 Citations

Scopus - 22 Citations

Other information

Authenticus ID: P-00Q-ZAC

DOI: 10.7554/elife.47646

Abstract (EN): According to the prevailing 'clock' model, chromosome decondensation and nuclear envelope reformation when cells exit mitosis are byproducts of Cdk1 inactivation at the metaphase-anaphase transition, controlled by the spindle assembly checkpoint. However, mitotic exit was recently shown to be a function of chromosome separation during anaphase, assisted by a midzone Aurora B phosphorylation gradient - the 'ruler' model. Here we found that Cdk1 remains active during anaphase due to ongoing APC/C-cd(c2)0 - and APC/C-cdh1 -mediated degradation of B-type Cyclins in Drosophila and human cells. Failure to degrade B-type Cyclins during anaphase prevented mitotic exit in a Cdk1-dependent manner. Cyclin B1-Cdk1 localized at the spindle midzone in an Aurora B-dependent manner, with incompletely separated chromosomes showing the highest Cdk1 activity. Slowing down anaphase chromosome motion delayed Cyclin B1 degradation and mitotic exit in an Aurora B-dependent manner. Thus, a crosstalk between molecular 'rulers' and 'clocks' licenses mitotic exit only after proper chromosome separation.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 31