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© Emmanuel Lemichez
Microscopy image showing the formation of large tunnels in a blood vessel endothelial cell induced by a group of bacterial toxins
Publication : Nature communications

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

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Nature communications - 03 Jan 2019

Vitiello E, Moreau P, Nunes V, Mettouchi A, Maiato H, Ferreira JG, Wang I, Balland M

Link to Pubmed [PMID] – 30604763

Nat Commun 2019 01;10(1):52

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 acto-myosin 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.

https://www.ncbi.nlm.nih.gov/pubmed/30604763