Cell Cycle Calculators

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The cell cycle is the ordered sequence of events by which a cell grows and divides into two daughter cells. It consists of four phases: G1 (first gap/growth phase), S (DNA synthesis/replication), G2 (second gap/growth phase), and M (mitosis/cell division). Cells can also exit the cycle into a quiescent state G0. The cycle is regulated by cyclin-dependent kinases (CDKs) activated by cyclins, tumor suppressors (RB, p53), and CKIs (CDK inhibitors). Three major checkpoints ensure fidelity: G1/S checkpoint (restriction point), G2/M checkpoint (DNA damage), and spindle assembly checkpoint (SAC) in mitosis.

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Cell Cycle Phases

  • G1 (10–12 hours): Cell growth; protein synthesis; integration of mitogenic signals; commitment at restriction point (R point)
  • S phase (6–8 hours): DNA replication; histone synthesis; genome is duplicated exactly once
  • G2 (3–5 hours): Continued growth; preparation for mitosis; DNA damage check
  • M phase (1 hour): Mitosis (prophase → metaphase → anaphase → telophase) + cytokinesis; sister chromatids separated to daughter cells
  • G0: Quiescence; cells exit cycle (neurons, muscle cells are permanently G0; most somatic cells can re-enter G1 on stimulation)

Cyclin-CDK Complexes

  • G1: Cyclin D-CDK4/6 → phosphorylates RB → releases E2F
  • G1/S: Cyclin E-CDK2 → completes RB phosphorylation → commitment to S phase
  • S: Cyclin A-CDK2 → drives DNA replication
  • G2/M: Cyclin B-CDK1 (MPF) → drives mitotic entry (nuclear envelope breakdown, chromosome condensation)

Checkpoints

G1/S (restriction point): checks DNA integrity and growth factor status; p53/p21 pathway. G2/M: checks DNA replication completion and DNA damage; ATM/ATR → CHK1/CHK2 → CDC25 inhibition. SAC (spindle assembly): checks kinetochore-microtubule attachment; BubR1, Mad2 → APC/C inhibition until all chromosomes are attached.

Glossary

Cell Cycle
The ordered sequence of G1 → S → G2 → M phases leading to cell division; regulated by cyclin-CDK complexes; monitored at G1/S, G2/M, and spindle assembly checkpoints.
Cyclin-CDK Complex
A regulatory kinase complex that phosphorylates target proteins to drive cell cycle progression; cyclin oscillates while CDK is stable; key complexes: D-CDK4/6 (G1), E-CDK2 (G1/S), B-CDK1 (M).
Spindle Assembly Checkpoint (SAC)
Ensures all chromosomes are kinetochore-attached before anaphase; unattached kinetochores generate MCC → inhibits APC/C → prevents sister chromatid separation; targeted by antimitotic cancer drugs.

Frequently Asked Questions

The cell cycle has four main phases: G1 (Gap 1): the cell grows, synthesizes proteins and organelles, and integrates extracellular signals. Duration: 10–12 hours in typical somatic cells. Ends at the restriction point when the cell commits to DNA replication. S phase (Synthesis): DNA is replicated exactly once; each chromosome is duplicated to form sister chromatids joined by cohesin. Duration: 6–8 hours. G2 (Gap 2): continued growth; preparation for mitosis (centriole duplication completes); DNA damage checkpoint. Duration: 3–5 hours. M phase (Mitosis): chromosomes condense, align at metaphase plate, and separate to daughter cells. Followed by cytokinesis (cytoplasm division). Duration: ~1 hour. G0: quiescent state; cells that have exited the cycle — permanently (neurons, muscle) or reversibly (fibroblasts await growth factors).

CDKs (cyclin-dependent kinases) are constitutively expressed kinases that are inactive without their cyclin partner. Cyclin levels oscillate during the cycle, activating CDKs at specific phases. Key complexes: Cyclin D-CDK4/6 (G1): activated by mitogenic signals; initiates RB phosphorylation → partial E2F release → transcription of cyclin E and other S-phase genes. Cyclin E-CDK2 (G1/S): completes RB hyperphosphorylation → full E2F release → irreversible commitment to S phase (restriction point). Cyclin A-CDK2 (S/G2): drives DNA replication; degrades cyclin E. Cyclin B-CDK1/MPF (M): triggers mitotic entry — nuclear envelope breakdown, chromosome condensation, spindle formation. After mitosis: APC/C (anaphase-promoting complex) ubiquitinates cyclins → proteasomal degradation → CDK inactivation → cycle reset.

The spindle assembly checkpoint (SAC, also called mitotic checkpoint) ensures that all chromosomes are properly attached to spindle microtubules at their kinetochores before anaphase begins. Mechanism: unattached kinetochores generate a 'wait anaphase' signal by recruiting the mitotic checkpoint complex (MCC = MAD2, BubR1, BUB3, CDC20). MCC inhibits APC/C (anaphase-promoting complex): APC/C cannot ubiquitinate securin → securin cannot be degraded → separase cannot cleave cohesin. Once all kinetochores are attached (bioriented): MCC is disassembled → APC/C activates → securin degraded → separase cleaves cohesin → sister chromatids separate → anaphase. Importance: SAC failure → chromosome segregation errors → aneuploidy → common in cancer (CIN: chromosomal instability). SAC is targeted by antimitotic drugs (taxol, vinblastine) — these drugs prevent microtubule dynamics → sustained SAC → cell cycle arrest → apoptosis.

Cancer results from loss of normal cell cycle checkpoint control through mutations in: RB pathway: RB is a tumor suppressor that prevents S phase entry. RB mutations (retinoblastoma), CDK4/CDK6 amplification, cyclin D1 overexpression (all inactivate RB) → constitutive S phase entry → uncontrolled proliferation. p53 pathway: p53 is mutated in > 50% of cancers → DNA-damaged cells can replicate → mutation accumulation → cancer progression. p16^(INK4a) (CDK4/6 inhibitor): deleted/silenced in many cancers → CDK4/6 constitutively active → RB phosphorylated → E2F free → proliferation. CDK4/6 inhibitors (palbociclib, ribociclib): approved drugs for HR+/HER2- breast cancer — restore G1 arrest by blocking CDK4/6 → preventing RB phosphorylation. APC/C (SAC): mutations in SAC components → chromosome instability → aneuploidy.