DNA Repair Kinetics: Breaks, Enzymes & Mutation Risk (2D)
A 2D kinetics lab: double-strand breaks arrive along a schematic DNA strand at a set rate, a Michaelis-Menten-saturated repair-enzyme pool clears them, and any break left unrepaired long enough converts into a permanent mutation.
Every cell constantly takes DNA damage, and this 2D companion turns the repair process into a live kinetics model rather than a decoration: double-strand breaks arrive along the strand as a Poisson process at the damage rate you set, and a fixed pool of repair enzymes clears them following Michaelis-Menten saturation — throughput rises with the backlog of breaks but plateaus once the enzyme pool is fully occupied, the same saturating behaviour real repair foci show under heavy damage. Any break that stays unrepaired for too long carries a constant per-second hazard of turning into a permanent mutation, and that hazard's timescale shortens as chromatin accessibility drops, mirroring why densely packed heterochromatin is harder for repair machinery to reach cleanly than open chromatin.
2D DNA-repair kinetics: Poisson-arriving double-strand breaks, a Michaelis-Menten-saturated enzyme pool, and an exponential per-break mutation hazard driven by chromatin accessibility. Adjustable damage rate, repair efficiency, chromatin accessibility and enzyme-pool size, plus a UV-pulse burst-damage event.
2D · HTML5 Canvas 2D · 60 FPS target · runs fully client-side, no install
The enzyme pool is modelled with Michaelis-Menten saturation: total repair throughput is Vmax·B/(Km+B), where B is the number of active breaks. Once B is much larger than the saturation constant, adding more breaks barely increases throughput because the enzyme pool is already working at capacity — the same saturation behaviour real repair foci show under heavy damage.
Each unrepaired break carries a constant per-second hazard of converting into a permanent mutation, modelled as an exponential process. Lower chromatin accessibility shortens the average time before that happens, because closed chromatin is harder for repair machinery to reach — matching why heterochromatic regions accumulate more unrepaired damage than open, accessible DNA.
It instantly adds a burst of 6-10 new double-strand breaks, mimicking a short high-dose exposure (UV, ionizing radiation) rather than the steady background damage rate — a good way to see the enzyme pool get temporarily overwhelmed and watch the mutation count climb.