Each polyp on the colony's branching lattice carries an epigenetic accessibility score A (0–1), a proxy for how "open" its chromatin is — how easily histone acetylation and DNA-demethylation can unlock developmental genes. It relaxes toward a target set by paracrine signal from wounded or already-reprogrammed neighbours:
signal = Σ (dead neighbours) + 0.5·Σ (stem/blastema neighbours)
A_target = plasticity · (damage·signal + 0.3·envStress)
dA/dt = (A_target − A) / τ
When A crosses a fixed reprogramming threshold, a healthy polyp dedifferentiates into a stem-like i-cell. After a residence time it becomes a proliferating blastema cell, which — once past its division time — either colonises an adjacent dead site with new redifferentiated tissue or, if no wound remains nearby, matures in place. High environmental stress independently raises the chance a healthy or newly regenerated polyp bleaches (pale, reduced vigour); a polyp that stays bleached too long can die, competing with the very regeneration the wound triggered.
- Strike colony — kills a cluster of polyps at a random point, sized by damage severity, and starts the cascade.
- Damage severity — how large and how strong the wound signal is.
- Environmental stress — thermal/pH stress; raises A_target but also drives bleaching risk, so too much "help" can backfire.
- Epigenetic plasticity — how readily chromatin opens in response to signal (histone acetylation / methylation turnover rate).
This mirrors the real biology: coral regeneration after breakage or predation proceeds by dedifferentiation of specialised cells into stem-like states, rapid proliferation of a blastema, and redifferentiation to rebuild lost structure — a process documented by RNA-Seq and single-cell transcriptomics and increasingly targeted by assisted-regeneration research.