Acto-myosin force organization modulates centriole separation and PLK4 recruitment to ensure centriole fidelity

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

Authors

Vitiello, E (Author) Other; Moreau, P (Author) Other; Nunes, V (Author) Other; Mettouchi, A (Author) Other; Maiato, H (Author) Other; J Ferreira (Author) FMUP; Wang, I (Author) Other; Balland, M (Author) Other

Journal

Title: Nature Communications

Vol. 10

ISSN: 2041-1723

Publisher: Springer Nature

Indexing

ISI Web of Knowledge - 9 Citations

Scopus - 11 Citations

Other information

Authenticus ID: P-00Q-303

DOI: 10.1038/s41467-018-07965-6

Abstract (EN): The presence of aberrant number of centrioles is a recognized cause of aneuploidy and hallmark of cancer. Hence, centriole duplication needs to be tightly regulated. It has been proposed that centriole separation limits centrosome duplication. The mechanism driving centriole separation is poorly understood and little is known on how this is linked to centriole duplication. Here, we propose that actin-generated forces regulate centriole separation. By imposing geometric constraints via micropatterns, we were able to prove that precise actomyosin force arrangements control direction, distance and time of centriole separation. Accordingly, inhibition of acto-myosin contractility impairs centriole separation. Alongside, we observed that organization of acto-myosin force modulates specifically the length of S-G2 phases of the cell cycle, PLK4 recruitment at the centrosome and centriole fidelity. These discoveries led us to suggest that acto-myosin forces might act in fundamental mechanisms of aneuploidy prevention.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 12