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#G2 phase

15 public questions tagged with this topic.

What happens if a proteasome inhibitor is added to cells in G2 phase?

Cell cycle progression relies heavily on ubiquitin-proteasome pathway to confer irreversibility to transitions via degradation of cyclins and CDK inhibitors. Proteasome comprises 20S catalytic core with chymotrypsin-like, trypsin-like, caspase-like activities and 19S regulatory particle recognizing polyubiquitinated proteins. Inhibitors such as MG132 peptide aldehyde, lactacystin, and clinically used bortezomib block catalytic threonine residues, causing accumulation of polyubiquitinated substrates. When applied in G2, proteasome blockade prevents degradation of SCF substrates like p21 and Wee

Ref: Ciechanover, Nature Reviews Mol Cell Biol 2005, Proteasome and Cycle. Alberts 7th ed., Chapter 3.

In which phase of the cell cycle do cells prepare for mitosis?

G2 phase operates as final growth and quality control interval preparing cells materially and regulatory for mitosis. After completion of DNA replication in S phase, cells enter G2 where synthesis continues: transcription of genes encoding tubulin isotypes, gamma-tubulin ring complex proteins gamma-TuRC, pericentrin, Cep192, and microtubule-associated proteins rises to stockpile building blocks for spindle assembly. Centrosomes duplicated in S phase mature by acquisition of pericentriolar material becoming competent microtubule organizing centers. Organelles including Golgi apparatus and mitoc

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 17, G2 Phase Preparation for Mitosis.

The G2 phase is characterized by:

G2 phase is second gap phase dedicated to growth, quality surveillance, and accumulation of components required for mitosis. After S phase completes DNA synthesis, cells continue protein synthesis, particularly tubulin alpha/beta heterodimers and gamma-tubulin ring complex proteins for spindle assembly, histone variants H2AZ for chromatin stability, and membrane lipid synthesis for organelle expansion. Centrosomes duplicated during S phase mature in G2 by recruitment of pericentriolar material including pericentrin, Cep192, and Cdk5Rap2, acquiring ability to nucleate large astral microtubule a

Ref: Alberts et al., Molecular Biology of the Cell, 7th ed., Chapter 17, G2 as Preparation for M Phase.

What is the role of cyclins in cell cycle regulation?

Cyclins constitute regulatory subunits that impose temporal order on constitutively expressed but inactive cyclin-dependent kinases. In mammals, D-type cyclins respond to mitogens via Ras-MAPK induction, E-type governs G1/S boundary, A-type controls S and G2 progression, B-type drives mitosis. Binding of cyclin to CDK induces conformational change in T-loop exposing activation site for phosphorylation by CAK complex CDK7-cyclin H-Mat1, stabilizing fully active kinase competent for substrate phosphorylation. Substrate specificity derives from cyclin hydrophobic patch interacting with RXL motifs

Ref: Morgan, The Cell Cycle: Principles of Control, Chapter 3: Cyclin-CDK Regulation. Alberts 7th ed., Chapter 17.

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 initiatio

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

Wee1 kinase inhibition in G2 phase leads to:

G2 progression is gated by inhibitory phosphorylation of master mitotic kinase CDK1 that prevents premature mitotic entry while last preparations complete. Nuclear kinase Wee1 and membrane-associated Myt1 phosphorylate CDK1 subunit within cyclin B-CDK1 complex at Tyr15 and Thr14 within ATP-binding loop, rendering kinase catalytically inactive despite abundant cyclin B synthesized during G2, allowing centrosome maturation, Golgi segregation, and DNA repair synthesis to proceed. At G2/M border, dual-specificity phosphatases Cdc25A/B/C remove these phosphates, causing explosive autoamplification

Ref: Harper & Elledge, Mol Biol Cell 2007, Wee1 Control. Alberts 7th ed., Chapter 17, CDK1 Regulation.