In lines expressing ALS/FTD-associated mutant FUS, increasing the abundance of these 8 M urea-soluble assemblies (e.g., by heat-stress-induced depletion of molecular chaperones) exacerbated motor deficits and accelerated mortality (Figure S9; p < 0.01; n = 16 animals/ strain). This evidence concerns the gene FUS and amyotrophic lateral sclerosis.