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#MPF

3 public questions tagged with this topic.

Cell Cycle Regulation

The M-phase regulator known as MPF (Maturation Promoting Factor) consists of:

Experiments in amphibian oocytes and in yeast genetics converged upon identification of universal M-phase regulator historically called Maturation Promoting Factor for its ability to induce meiotic maturation when cytoplasm from M-phase cells injected into G2 oocytes. Molecular composition resolved as complex of catalytic subunit CDK1 originally named cdc2 or p34cdc2 and regulatory subunit Cyclin B. CDK1 provides serine-threonine kinase activity requiring activating phosphorylation on activation loop Thr161 by CAK complex CDK7-Cyclin H-MAT1 and removal of inhibitory phosphates Thr14 Tyr15 via

Ref: Nurse, Universal Control of Cell Division by CDK1-Cyclin B MPF, Nature 1990; Alberts et al., Molecular Biology of the Cell, Chapter 17, Discovery of MPF.

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Cell Cycle Regulation

The mitotic CDK1-Cyclin B complex (MPF) is responsible for:

MPF converts interphase architecture into mitotic state through phosphorylation of hundreds of substrates. Nuclear entry of CDK1-Cyclin B, facilitated by phosphorylation of Cyclin B cytoplasmic retention sequence, allows access to chromatin proteins. Condensin I and II pentameric complexes containing SMC2, SMC4 become phosphorylated at non-SMC subunits CAP-D2, D3, CAP-G, H2, activating ATP-dependent loop extrusion that folds 10nm fiber into 700 nm wide rod chromosomes. Lamins phosphorylated at Ser22 Ser392 disassemble intermediate filament meshwork leading to nuclear envelope breakdown and mer

Ref: Hirano, Condensins and Mitotic Chromosome Architecture, Nat Rev Mol Cell Biol 2012; Alberts et al., Chapter 17, MPF Targets.

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Cell Cycle Regulation

Which complex regulates the G2/M transition?

G2 to M transition represents bistable switch controlled by accumulation of active CDK1-Cyclin B, often termed mitosis-promoting factor. Throughout G2, Cyclin B synthesis steadily rises transcribed by FoxM1 and stabilized, yet associated CDK1 remains inactive due to inhibitory phosphorylations at Thr14 and Tyr15 catalyzed by nuclear Wee1 and cytoplasmic Myt1 kinases occupying ATP-binding pocket. At threshold, dual specificity phosphatase Cdc25B initially and subsequently Cdc25C removes these phosphates. Activating Thr161 phosphorylation by CAK complex CDK7-Cyclin H further boosts activity. Onc

Ref: Morgan, Cell Cycle Control Principles of G2/M Transition, Chapter 3; Alberts et al., Molecular Biology of the Cell, CDK1-Cyclin B Regulation.

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