Abstract
EVER SINCE ITS DISCOVERY in 1997 (11), myostatin and its negative effects on skeletal muscle mass have understandably captivated many biomedical, agricultural, and comparative biologists, since the gains in muscle mass associated with the myostatin null phenotype have never been reproduced by the administration of growth promoters regardless of species or mode of administration (9). The potential benefits of reproducing these effects in the clinic or in animal feed lots are obvious and cannot be overestimated. Relieving myostatin’s restrictive effects on skeletal muscle growth and development could revolutionize the clinical treatment of different muscle growth disorders, including some muscular dystrophies (1‐3, 16), and has the potential to significantly enhance the production of meat animal products as well (4, 6, 7, 10, 12). However, myostatin’s functions are poorly defined in nonmammalian vertebrates and may be quite different in the fishes where multiple gene copies are differentially expressed in many tissues (5, 8, 13‐15). This is in stark contrast to mammals where myostatin expression is limited primarily to skeletal muscle and suggests that its functions in fish may be as diverse as its expression pattern. Thus, animal scientists and comparative biologists alike are greatly interested in extrapolating information between different animal models. This has proven quite difficult, however, as the current nomenclature for members of this transforming growth factor- subfamily, which also includes growth differentiating factor (GDF)-11, is often confusing and sometimes problematic.
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