Self-organized flows and droplet swimming drive rapid fibril formation from ATP condensates

Biomolecular condensates are central to cellular physiology, yet their pathological aging into fibrillar aggregates underlies neurodegenerative diseases such as ALS and other disorders of protein aggregation. Yet, this process remains poorly understood and is typically assumed to be a slow and passive process. Here, we show that one of the simplest building blocks of life, Adenosine 5'-triphosphate (ATP), can form condensates that undergo rapid aging in macromolecularly crowded environments, transforming from liquid droplets to urchin-like fibrillar aggregates. Using experiments and theory, we report a suite of previously unrecognized mechanisms of fibril aggregation from droplets, including wetting-induced engulfment, self-organized flows within condensates and directed droplet swimming (dialytaxis). These behaviors originate from Marangoni flows triggered by ATP fibrillization, which accelerate aging dynamics and demonstrate that condensate aging is an active process. These findings uncover fundamental physical principles underlying condensate aging and offer broadly relevant insights into neurodegenerative diseases, bio-inspired material engineering, and soft matter physics.