Analysis of metabolome and transcriptome of longissimus thoracis and subcutaneous adipose tissues reveals the regulatory mechanism of meat quality in MSTN mutant castrated male finishing pigs

The underlying mechanism of myostatin (MSTN) gene mutation impact on porcine carcass and meat quality has not yet been fully understood. The meat quality trait testing of the second filial generation wild-type (WT) and homozygous MSTN mutant (MSTN-/-) castrated male finishing pigs, and RNA-seq and metabolomics on the longissimus thoracis (LT) and subcutaneous adipose tissues (SAT) were performed. Compared with WT pigs, MSTN-/- pigs had higher carcass lean percentage and lower backfat thickness (all P < 0.01), and also had lower shear force (P < 0.01) and meat redness (P < 0.05). The gene and metabolite expression profiles were different between two groups. Metabolites and genes related to purine metabolism (such as xanthine metabolite (P < 0.05), AMPD3 and XDH genes (all padj < 0.01)), PI3K/Akt/mTOR signaling pathway (such as Phe-Phe and Glu-Glu metabolites (all P < 0.05), WNT4 and AKT2 genes (all padj < 0.01)), antioxidant related pathway (such as GPX2, GPX3, and GPX7 genes (all padj < 0.01)), and extracellular matrix related pathway (such as COL1A1 and COL3A1 genes (all padj < 0.01)) were significantly altered in LT. While metabolites and genes associated to lipid metabolism (such as trans-elaidic acid and PE(18:1(9Z)/0:0) metabolites (all P < 0.05), ACOX1, ACAT1 and HADH genes (all padj < 0.01)) were significantly changed in SAT. This study revealed the biological mechanisms of homozygous MSTN mutation regulated porcine carcass and meat quality, such as lean meat percentage, fat deposition and tenderness, which provides reference for the utilization of MSTN-/- pigs.