The Mitotic Exit Network and Cdc14 phosphatase initiate cytokinesis by counteracting CDK phosphorylations and blocking polarised growth.

摘要: Polarisation of the actin cytoskeleton must cease during cytokinesis, to support efficient assembly and contraction actomyosin ring at site cell division, but underlying mechanisms are still understood poorly in most species. In budding yeast, Mitotic Exit Network (MEN) releases Cdc14 phosphatase from nucleolus anaphase, leading inactivation mitotic forms cyclin-dependent kinase (CDK) onset septation, before G1-CDK can be reactivated drive re-polarisation a new bud. Here, we show that premature CDK, release Cdc14, allows divert away polarised growth, thereby delaying progression through cytokinesis. Our data indicate cells normally avoid this problem via MEN-dependent which counteracts all classes CDK-mediated phosphorylations cytokinesis blocks growth. The dephosphorylation CDK targets is therefore central mechanism by MEN initiate block growth late mitosis.