In striated muscle, X-ROS is the mechanotransduction pathway by which mechanical stress
transduced by the microtubule network elicits reactive oxygen species. X-ROS tunes Ca2+
signalling in healthy muscle, but in diseases such as Duchenne muscular dystrophy (DMD),
microtubule alterations drive elevated X-ROS, disrupting Ca2+ homeostasis and impairing
function. Here we show that detyrosination, a post-translational modification of α-tubulin,
influences X-ROS signalling, contraction speed and cytoskeletal mechanics. In the mdx …