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The early embryonic Xenopus cell cycles are characterized by alternating oscillations of Cyclin-dependent kinase-1 (Cdk1) and Anaphase Promoting Complex/Cyclosome (APC/C) activities. The early cycles before midblastula transition lack significant inhibitory Cdk1 phosphorylations and are driven by periodic accumulation of Cyclin B before M phase and its degradation by APC/C at the end of M phase. Both experiments and mathematical modelling suggest that while Cdk1:CycB phosphorylation activates APC/C, it inhibits its co-activator Cdc20 (Fizzy). These interactions create an amplified negative-feedback loop which is at the heart of all cell cycle oscillations. Recent experiments find that the APC/C inhibitor, Emi2/XErp1 is essential for large amplitude and short period Cyclin B oscillations during early divisions in the intact Xenopus embryo. This finding is counter-intuitive since larger amplitudes should come with slower cycle times. We explain this paradox by analysing the amplified negative feedback model extended with APC/C inhibition by Emi2. We show that Emi2 interferes with the intrinsic time-delay in APC/C activation and inactivation to increase the amplitude as well as shorten the period of Cyclin B oscillation.

Original publication

DOI

10.1016/j.bpc.2013.03.002

Type

Journal article

Journal

Biophys Chem

Publication Date

07/2013

Volume

177-178

Pages

1 - 6

Keywords

Anaphase-Promoting Complex-Cyclosome, Animals, CDC2 Protein Kinase, Carboxylic Ester Hydrolases, Cdc20 Proteins, Cell Cycle, Cell Cycle Proteins, Cyclin B, F-Box Proteins, Models, Theoretical, Oocytes, Phosphorylation, Ubiquitin-Protein Ligase Complexes, Xenopus, Xenopus Proteins