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Muscle injury can sometimes occur with a sudden, inconsiderate movement. Unlike other tissues, such as bone, muscles are not efficient at repair.

Regeneration of the muscle requires complex coordination between several different processes. The key player in muscle repair is the muscle stem cells, which divide and produce new muscle cells to fix the muscle damage. A crucial regulator of muscle function and repair is a ‘signaling molecule’ called calcineurin.

Calcineurin accomplishes its effect on muscle by inhibiting another protein called FoxO, which is a protein that plays a crucial role in skeletal muscle atrophy through the induction of genes involved in cell cycle repression and protein degradation. Suppressing the effects of FoxO, calcineurin ensures that proliferating cells stay alive and keep dividing to produce enough cells to repair muscle damage.

Researcher Nadia Rosenthal, head of European Molecular Biology Laboratory’s Mouse Biology Unit, and her team found a naturally occurring version of calcineurin, called CnAB1. CnAB1 has the unique property of RNA splicing. When the gene has been copied from DNA into RNA, certain pieces of information are cut out of the RNA molecule and does not make part of the protein, which is why CnAB1 lacks a regulatory site that normally represses its activity.

CnAB1 is permanently active and disconnects the protein’s activity from the normal injury signals. Free of regulation, CnAB1 is flexible in its reaction to muscle injury. Permanently active CnAB1 is expressed only in proliferating stem cells and regenerating muscles, suggesting something like an emergency response team that is called only in response to muscle damage.

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