A new role for foxm1 in zebrafish muscle homeostasis and consequences of Cas9 overexpression in vivo
foxm1is a master regulator of the cell cycle but recent data have suggested that this transcription factor also modulates gene networks associated with other cellular mechanisms. In their recent work, a team led by Elsa Logarinho and José Bessa from i3S used CRISPR/Cas9 to disrupt foxm1 in the zebrafish terminally differentiated fast-twitching muscle cells. They observed that Cas9 expression alone was strongly deleterious to muscle cells, inducing apoptosis. Interestingly, disruption of foxm1 increased myofiber death and contributed to non-autonomous satellite cell activation and proliferation. The report was published on Cells with the title “foxm1 Modulates Cell Non-Autonomous Response in Zebrafish Skeletal Muscle Homeostasis” and suggests a new function for foxm1 in muscle non-autonomous response to myofiber death, in zebrafish.