Epistatic Capacitance

Theory project on how bottleneck-induced allele frequency changes convert epistatic variance (V_I) into additive variance (V_A) vs selection pathway (V_I → Δμ). Andres Barboza lead.

Status: active

Current hypothesis:

During population bottlenecks, selection-mediated conversion of epistatic variance (V_I → Δμ) dominates over drift-mediated conversion (V_I → V_A) as the primary mechanism releasing hidden variation, with the relative contribution of each pathway scaling predictably with bottleneck severity and pre-bottleneck V_I magnitude. The 85–90% epistatic contribution to Δμ observed in simulations implies that bottleneck populations are more phenotypically displaced than classical additive models predict.

Next action:

Andres to complete LxS simulations and finalize manuscript