Progression through the cell cycle is driven by cyclins that rise and fall in sequence, each binding a cyclin-dependent kinase (CDK) to form an active complex. Cyclin D/CDK4-6 pushes the cell through G1 and phosphorylates Rb; cyclin E/CDK2 peaks at the G1→S boundary and licenses DNA replication; cyclin A/CDK2 drives S-phase and prepares G2; cyclin B/CDK1 (the classic "MPF") triggers nuclear envelope breakdown and chromosome condensation at the start of M.
progress += (dt / cycleLength) · speed
if damage ≥ apoptosisThreshold at a checkpoint → apoptosis
elif damage ≥ arrestThreshold at a checkpoint → arrest, hold progress
else → pass, continue to next phase
- Cycle speed — how fast the cell advances through G1→S→G2→M when no checkpoint is holding it back.
- Damage severity — how much DNA damage each click of "Inflict DNA damage" adds (capped at 100%); damage decays slowly on its own, modelling repair enzymes at work.
- Inflict DNA damage — simulates a mutagenic hit; the next checkpoint the cell reaches (G1/S, G2/M, or the spindle-assembly checkpoint in M) will hold the cycle arrested while damage is above threshold, or send the cell into apoptosis if damage is severe.
- Reset — clears damage and restarts the cycle from early G1.
Real-world relevance: mutations that disable these checkpoints (e.g. in the p53 or Rb pathways) let damaged DNA slip through into daughter cells — this is exactly the mechanism behind most cancers, which is why cyclins, CDKs and checkpoint proteins are major drug targets in oncology.