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Skeletal muscle has a remarkable capacity to regenerate, researchers from Brigham and Women’s Hospital bombarded zebrafish with chemical mutagen and screened for larvae with defective skeletal muscle structure. To investigate the mechanism behind skeletal muscle growth and regeneration, using genetic mapping, they found that zebrafish larvae with a mutation in DDX27 showed reduced muscle growth and impaired regeneration.
Controlling protein synthesis in muscles may allow the development of effective targeted treatments for skeletal muscle diseases. Loss of muscle mass is a debilitating feature that is a common manifestation of a wide array of diseases, and leads to reduced muscle function and increased morbidity and mortality. Maintenance of skeletal mass relies on a dynamic balance between protein synthesis and degradation.
Conditions like myopathies, sarcopenia, cancer cachexia, disuse atrophy, sepsis and chronic kidney diseases can lead to a disruption of this balance in favor of reduced protein synthesis. The researchers discovered that DDX27 is involved in ribosome biogenesis and protein synthesis in skeletal muscle. Loss of DDX27 affects the function of skeletal muscle by disrupting the regulation and production of proteins that are crucial for muscle function. Promoting muscle growth in patients with skeletal muscle disorders may restore muscle strength, mobility and reducing morbidity.
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