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Rheostatic Network Consolidation Drives Physical Aging in Biomolecular Condensates

Polanco, D.; Pele, K. G.; Mairo, A.; Martinez-Monge, M.; Moreno, N.; Cremades, N.

2026-07-05 biophysics
10.64898/2026.06.30.735561 bioRxiv
Show abstract

While the physical aging of biomolecular condensates into macroscopic glasses is heavily linked to pathological disease states, the nanoscale topological rules governing this non-equilibrium relaxation remain elusive. Using heterotypic alpha-synuclein-Tau coacervates, we combine variable-stringency dissolution and FLIM-FRET to provide direct experimental mapping of the internal network reorganization over time. Rather than a passive, isotropic kinetic jamming event typical of classic glasses, we demonstrate that this physical aging is driven by continuous rheostatic network consolidation; a progressive, directed topological relaxation toward deeper free-energy minima powered by the cooperative spatial optimization of sticker motifs. We formalize these dynamics into a mesoscale series-resistance model derived from size-resolved kinetics, proving that thermodynamic quench depth dictates the initial network state while clustered sticker patterning introduces configurational frustration that kinetically stalls maturation to preserve liquidity. This multi-scale framework links sequence grammar to non-equilibrium transport laws, revealing how biomolecular assemblies navigate the boundary between physiological utility and pathological arrest.

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