Integrative Analysis of Blood Transcriptomics and Metabolomics Reveals Molecular Regulation of Backfat Thickness in Qinchuan Cattle

SIMPLE SUMMARY: Subcutaneous fat deposition in cattle has become the focus of breeders’ attention because excessive deposition is not conducive to efficient feed conversion. In the present study, based on the results of blood transcriptome sequencing and the detection of metabolites, bioinformatic analysis was used to explore the differential genes and metabolites associated with the subcutaneous fat depot phenotype of beef cattle. In conclusion, the functional genes SMPD3 and CERS1, as well as the metabolite sphingosine 1-phosphate, were identified as an important metabolite and candidate genes to account for the differences in phenotype. These differential genes and the metabolite are thought to have an important reference value for effective breeding to improve beef performance. ABSTRACT: A crucial goal of reducing backfat thickness (BFT) is to indirectly improve feed conversion efficiency. This phenotype has been reported in certain papers; however, the molecular mechanism has yet to be fully revealed. Two extreme BFT groups, consisting of four Qinchuan cattle, were chosen for this study. We performed metabolite and transcriptome analyses of blood from cattle with a high BFT (H-BFT with average = 1.19) and from those with a low BFT (L-BFT with average = 0.39). In total, 1106 differentially expressed genes (DEGs) and 86 differentially expressed metabolites (DEMs) were identified in the extreme trait. In addition, serum ceramide was strongly correlated with BFT and could be used as a potential biomarker. Moreover, the most notable finding was that the functional genes (SMPD3 and CERS1) and metabolite (sphingosine 1-phosphate (S1P)) were filtered out and significantly enriched in the processes related to the sphingolipid metabolism. This investigation contributed to a better understanding of the subcutaneous fat depots in cattle. In general, our results indicated that the sphingolipid metabolism, involving major metabolites (serum ceramide and S1P) and key genes (SMPD3 and CERS1), could regulate BFT through blood circulation.