Clock Gene Network Simulator: Molecular Circadian Oscillator Model

simulator intermediate ~10 min
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T = 24.2 h — robust circadian oscillation

With default parameters, the Goodwin oscillator produces a stable 24.2-hour period with PER/CRY protein peaking ~6 hours after CLOCK/BMAL1 peak, closely matching mammalian circadian timing.

Formula

dM/dt = k_t × Math.pow(K, n) / (Math.pow(K, n) + Math.pow(P, n)) - k_dm × M — mRNA dynamics with Hill repression
dP/dt = k_tl × M - k_d × P — protein translation and degradation
H(P) = Math.pow(K, n) / (Math.pow(K, n) + Math.pow(P, n)) — Hill repression function

The Molecular Clockwork

At the heart of every cell in your body ticks a molecular clock — a self-sustaining oscillator built from interlocking feedback loops of gene transcription and protein degradation. The core loop centers on four gene families: CLOCK and BMAL1 (the activators) and PER and CRY (the repressors). CLOCK/BMAL1 heterodimers bind E-box promoter elements to drive PER and CRY transcription. The resulting proteins accumulate over hours, complex together, translocate to the nucleus, and directly inhibit CLOCK/BMAL1 — silencing their own genes. As PER/CRY are degraded by proteasomes, the brake lifts and the cycle begins anew.

The Goodwin Oscillator

Brian Goodwin's 1965 model distilled this feedback into its mathematical essence: a molecule that represses its own production through a nonlinear (Hill-type) function, with time delays introduced by intermediate steps. The critical requirement for sustained oscillation is sufficient nonlinearity — the Hill coefficient must exceed a threshold that depends on the number of intermediate steps. This simulation implements a refined Goodwin model calibrated to mammalian circadian parameters, showing how transcription rate, degradation rate, and cooperativity jointly determine period and amplitude.

Period-Determining Mechanisms

The approximately 24-hour period is not hardwired into any single rate constant — it emerges from the concert of many. However, certain steps are particularly influential. Casein kinase 1ε (CK1ε) phosphorylation of PER proteins marks them for ubiquitination and proteasomal degradation. The tau mutation in hamster CK1ε accelerates PER degradation, shortening the period to 20 hours. In humans, a PER2 mutation that removes the CK1ε phosphorylation site causes Familial Advanced Sleep Phase Syndrome — people who fall asleep at 7 PM and wake at 3 AM, running on a ~22-hour clock.

Robustness and Fragility

The circadian clock is remarkably robust to perturbations in most parameters — a property called structural stability. Temperature compensation keeps the period nearly constant from 25°C to 37°C (unlike most biochemical reactions that accelerate with heat). Yet the clock is exquisitely sensitive to light input, which can shift its phase by hours — the basis for entrainment to the solar cycle. This simulation reveals the parameter space where oscillations are robust versus the boundaries where rhythmicity collapses.

FAQ

How does the molecular clock work?

The core clock is a transcription-translation feedback loop (TTFL). CLOCK and BMAL1 proteins form a heterodimer that activates transcription of Period (PER) and Cryptochrome (CRY) genes. PER and CRY proteins accumulate, form complexes, enter the nucleus, and inhibit CLOCK/BMAL1 — shutting off their own production. As PER/CRY degrade, inhibition lifts and the cycle restarts. This takes ~24 hours.

What is the Goodwin oscillator model?

The Goodwin oscillator (1965) is a minimal mathematical model of a negative feedback gene regulatory loop with time delay. A gene product represses its own transcription via a Hill function. With sufficient cooperativity (Hill coefficient > ~8 in the original 3-variable model, or lower with additional variables), the system oscillates. It remains the foundation for computational circadian biology.

Why is the period approximately 24 hours?

The ~24-hour period emerges from the interplay of transcription rates, translation delays, protein stability, nuclear transport times, and post-translational modifications (phosphorylation, ubiquitination). Evolution has tuned these rate constants to match the solar day. CK1δ/ε phosphorylation of PER is a key period-determining step — mutations here cause human sleep disorders with shortened or lengthened periods.

What happens when clock genes are mutated?

Clock gene mutations cause dramatic phenotypes: the tau mutation in hamster CK1ε shortens the period to 20 hours, CLOCK Δ19 mice have a 27-hour period, PER2 mutations cause Familial Advanced Sleep Phase Syndrome (waking at 3–4 AM), and BMAL1 knockout mice are completely arrhythmic with accelerated aging.

Sources

Embed

<iframe src="https://homo-deus.com/lab/circadian-biology/clock-gene-network/embed" width="100%" height="400" frameborder="0"></iframe>
View source on GitHub