Fetal muscle development, mesenchymal multipotent cell differentiation, and associated signaling pathways.

Enhancing muscle growth while reducing fat accumulation improves the efficiency of animal production. The fetal stage is crucial for skeletal muscle development. Fetal muscle development involves myogenesis, adipogenesis, and fibrogenesis from mesenchymal multipotent cells (MC), which are negatively affected by maternal nutrient deficiencies. Enhancing myogenesis increases the lean-to-fat ratio of animals, enhancing intramuscular adipogenesis increases intramuscular fat that is indispensible for the superior eating properties of meat because fat is the major contributor to meat flavor. The promotion of fibrogenesis leads to the accumulation of connective tissue, which contributes to the background toughness of meat and is undesirable. Thus, it is essential to regulate MC differentiation to enhance lean growth and improve meat quality. To date, our understanding of mechanisms regulating the lineage commitment of MC is limited. In this review, we first discuss the impact of maternal nutrient deficiency on fetal development, offspring body composition, and meat quality. Because maternal nutrition affects fetal muscle through altering MC differentiation, we then review several important extracellular morphogens regulating MC differentiation, including hedgehog, Wingless and Int (Wnt), and bone morphogenic proteins. Possible involvement of epigenetic modifications associated with histone deacetylases class IIa and histone acetyltransferase, p300, in MC differentiation is also discussed.