Résumé
Mnk1 is a serine/threonine kinase identified as a target for MAP kinase pathways. Using chemical drug, kinase-dead expression or knock down by RNA interference, we show that inhibition of Mnk1 induces the formation of multinucleated cells, which can be rescued by expressing an RNA interference resistant form of Mnk1. We found that active human Mnk1 localises to centrosomes, spindle microtubules and the midbody. Time-lapse recording of Mnk1 depleted cells display cytokinesis defects, as daughter cells fuse back together. Under inhibition of Mnk1 activity, no microtubule defect at the midbody was detected, however membrane vesicles anchorage at the midbody was impaired as lumenal-GFP positive-vesicles did not accumulate at the midbody. At the molecular level, we found that centriolin localisation was impaired at the midbody in Mnk1 depleted cells. As a consequence endobrevin, a V-SNARE protein implicated in the abscission step, was not properly localised at the midbody. Altogether our data show that Mnk1 activity is required for abscission.