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Model scenarios for switch‐like mitotic transitions
Author(s) -
Vinod P.K.,
Novak Bela
Publication year - 2015
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2015.02.007
Subject(s) - protein phosphatase 2 , phosphatase , cyclin dependent kinase 1 , mitosis , microbiology and biotechnology , mitotic exit , phosphorylation , kinase , chemistry , substrate (aquarium) , maturation promoting factor , biology , biochemistry , biophysics , cell cycle , cell , ecology , anaphase
To facilitate rapid accumulation of Cdk1‐phosphorylated substrate proteins, the Cdk1 counter‐acting phosphatase, PP2A‐B55 is inhibited during M phase by stoichiometric inhibitors (ENSA and Arpp19). These inhibitors are activated when phosphorylated by Cdk1‐activated Greatwall‐kinase. Recent experiments show that ENSA is dephosphorylated and inactivated by the PP2A‐B55 itself, and acts as an unfair substrate inhibiting PP2A‐B55 activity towards other Cdk1 substrates. Mathematical modelling shows that this mutual antagonism between the phosphatase and its inhibitor is insufficient to explain the switch‐like characteristics of mitotic entry and exit. We show that the feedback regulation of Greatwall activating kinase and/or inactivating phosphatase can explain the abruptness of these cell cycle transitions.