Transcriptional knock-down of mstn encoding myostatin improves muscle quality of Nile tilapia (Oreochromis niloticus)

Abstract

Abstract Background Myostatin (encoded by mstn) negatively regulates skeletal muscle mass and affects lipid metabolism. Relieving the inhibitory effect of mstn on growth can improve the muscle yield of teleost fishes. To explore the regulatory effects of mstn on muscle development and lipid metabolism in Nile tilapia (Oreochromis niloticus), we used antisense RNA to transcriptionally knock-down mstn. At 180 d, the body weight and body length were significantly higher in the mstn-knock-down group than in the control group (p < 0.05). Hematoxylin–eosin staining revealed that fish in the mstn-knock-down group exhibited myofiber hyperplasia but not hypertrophy. Oil red O staining revealed a remarkable increase in the area of lipid droplets in muscle in the mstn-knock-down group compared with that in the control group (p < 0.05). Nutrient composition analyses of muscle tissue showed that the crude fat content was significantly increased in the mstn-knock-down group (p < 0.05). The contents of saturated fatty acids, monounsaturated fatty acids, and polyunsaturated fatty acids were all significantly increased in the mstn-knock-down group (p < 0.05). Comparative transcriptome analyses revealed 2,420 significant differentially expressed genes between the mstn-knock-down group and the control group, including 1,055 up-regulated genes and 1,365 down-regulated genes. Among them, genes related to myoblast differentiation and lipid metabolism were enriched in fatty acid degradation, glycerolipid metabolism, and peroxisome proliferator activated receptor (PPAR) signaling pathways. The accuracy of the RNA-seq data was confirmed by qRT-PCR analyses. Our results indicate that disruptions to fatty acid degradation, glycerolipid metabolism, and the PPAR signaling pathway affect muscle development and lipid metabolism in mstn-knock-down Nile tilapia: acaa2, eci1, and lepr were remarkably up-regulated, and acadvl, lpl, foxo3, myod1, myog, and myf5 were significantly down-regulated (p < 0.05). These results show that knock-down of mstn results in abnormal lipid metabolism, acceleration of skeletal muscle development, and increased adipogenesis and weight gain in Nile tilapia.