Skip to content

#M phase

2 public questions tagged with this topic.

Which phase of the cell cycle is the most metabolically active?

Cellular metabolism is tightly coupled to cell cycle progression, with G1 phase exhibiting maximal biosynthetic activity to support doubling of mass before DNA replication. Upon growth factor binding, PI3K-Akt-mTORC1 pathway stimulates glucose uptake through GLUT1, increases glycolytic flux and pentose phosphate pathway for nucleotide precursors, enhances mitochondrial biogenesis via PGC1-alpha and mitochondrial transcription factor TFAM, and activates ribosome biogenesis through RNA polymerase I mediated rDNA transcription and S6K phosphorylation of ribosomal protein S6. Translation initiation factor eIF4E cap-binding protein synthesizes cyclins, CDKs, replication factors Cdt1, Cdc6, and histone chaperones. Lipid synthesis provides membrane for organelle growth, while amino acid transport sustains protein synthesis. By contrast, S phase devotes resources to dNTP synthesis, M phase shuts transcription, and G0 quiescent cells greatly reduce metabolic rate. Therefore G1 concentrates growth, accumulating tubulin, actin, and centrosome components monitored by size-sensing pathways. This circuitry is highly conserved across eukaryotes, integrating growth factor signals, DNA damage surveillance, and developmental cues, and its disruption frequently underlies oncogenesis, providing targets for checkpoint inhibitors and cancer therapeutics.

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 17: G1 Metabolism and Growth.

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 Cdc25 phosphatase. Cyclin B synthesized during S and G2 accumulates at G2/M, contains destruction box recognized by APC/C-Cdc20 for degradation providing temporal restriction, supplies cyclin box for CDK activation and contributes substrate docking through hydrophobic patch recognizing RXL motifs plus nuclear localization signal translocating complex into nucleus at prophase. MPF substrates include lamins causing envelope breakdown, condensin subunits driving chromosome compaction, microtubule regulators forming bipolar spindle and APC/C components regulating exit. Degradation of Cyclin B at anaphase inactivates MPF, allowing phosphatases to restore interphase state.

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.