Supplemental Tables Milovanovic et al

Similar to mammals, zebrafish repair skeletal muscle through a multi-step process that involves satellite cell activation, differentiation of progenitor cells into myocytes, their fusion into myotubes, followed by myotube maturation and myofiber hypertrophy. Coordination and timely regulation of these events are essential for functional muscle recovery. Here we identify <i>ankrd1a</i>, a gene responsive to muscle stress, as a new player in the repair of adult zebrafish skeletal muscle and show its involvement in modulating molecular mechanisms behind myogenic cell differentiation. It is expressed in newly forming muscle fibers from the stage of myoblast-like cells to their differentiation into mature myofibers, as well as in the apparently intact muscle fibers that surround the injury. Loss of <i>ankrd1a</i> function alters regulatory pathways involved in muscle cell differentiation, contraction, and myocyte fusion, leading to the acceleration of myogenic differentiation. Our data point to <i>ankrd1a</i> as a novel marker of newly forming myofibers and a hallmark of the adaptive process occurring in the intact myofibers that are in contact with wounded tissue. Without affecting the main regulatory networks, <i>ankrd1a</i> fine-tunes skeletal muscle repair by preventing premature myogenic differentiation during injury repair, which itself could impair functional recovery.