Long form leptin receptor and SNP effect on reproductive traits during embryo attachment in Suzhong sows

To ascertain whether the long form leptin receptor (LEPR) affects the regulation of embryo attachment and whether there are LEPR Single Nucleotide Polymorphisms (SNPs) associated with reproductive traits in pigs, Real-time qPCR was used to detect relative abundance of LEPR mRNA pattern in different tissues of Suzhong sows during the embryo attachment period (pregnancy day 13, 18 and 24) to the uterus, and PCR-RFLP as well as PCR-sequencing were used to investigate the coding sequence for SNPs of LEPR in a population of 512 Suzhong sows. Real-time qPCR results indicated that LEPR mRNA was present in all 22 tissues of pigs with differences in relative abundance of the LEPR mRNA (P < 0.05). Among these tissues, the greatest relative abundance occurred at the endometrial attachment site (P < 0.01), followed by the hypothalamus and most reproductive tissues (P < 0.05), and there was a lesser relative abundance of the LEPR mRNA in the pituitary. During different embryo attachment periods, LEPR mRNA was greatest on Day 18 (attachment; P < 0.05), followed by Day 24 (post-attachment), and relative abundance was least on Day 13 (pre-attachment). The prevalence of the LEPR mRNA in pregnant sows was greater than in non-pregnant sows (P < 0.05). At the c.2856C > T locus of LEPR, Chi-square test results demonstrated that allele and genotype frequencies were in Hardy-Weinberg disequilibrium at this locus, PCR-RFLP results revealed that Genotype TT was greater than Genotype CC (P < 0.05) for reproductive traits of TNB (Total Number Born) and NBA (Number Born Alive), which suggested that T allele at c.2856C > T locus has advantageous effects on litter size and litter weight in Suzhong pigs. In conclusion, the expression of the LEPR gene might be involved in the regulation of embryo attachment mechanisms in pigs, and the LEPR SNP c.2856C > T could be a molecular marker for improving litter size and litter weight in pig breeding.