FUS

Summary This study shows that disease-associated FUS mutations cause mitochondrial shortening and fragmentation in neurons, leading to neurotoxicity. The findings connect FUS dysfunction to mitochondrial dynamics, providing a potential mechanism for neurodegeneration in ALS patients carrying FUS mutations.

Summary CLIP-seq analysis reveals that FUS, an ALS-associated RNA-binding protein, preferentially binds to highly conserved intronic sequences of genes encoding other RNA-binding proteins in neurons. This autoregulatory network suggests a mechanism by which FUS dysfunction could broadly disrupt neuronal RNA metabolism.