Genetic effect and combined genotype effect of ESR, FSHß, CTNNAL1 and miR-27a loci on litter size in a Large White population.

To select new Large White line with high number of piglets born, genotypes of estrogen receptor (ESR), the follicle stimulating hormone ß subunit (FSHß), catenin alpha like 1 (CTNNAL1) and miR-27a were tested in 472 Large White sows. The associations of different genotypes with litter size traits were also studied. The results showed ESRBB and FSHßBB sows produced 0.41-1.49 more pigs per litter (p < .05) for total number born (TNB) and number born alive (NBA) than did other corresponding genotypes. TNB of CTNNAL1CG sows is 0.50 more pigs per litter (p < .05) than that of CTNNAL1GG sows with the dominance effect of 0.25 pigs per litter (p < .05). miR-27aBB sows had a less estimated breeding value (EBV) to TNB and had a more number of mummified pigs (NM) than did miR-27aAA or miR-27aAB sows (p < .05). Therefore, ESRB, FSHßB, CTNNAL1G, miR-27aA allele was favorable for litter size traits. Furthermore, combined genetic effect analysis showed ESRAAFSHßBB, ESRAACTNNAL1CG, ESRAAmiR-27aAA, FSHßBBCTNNAL1CC, FSHßBBmiR-27aAA and CTNNAL1CG miR-27aAB was the favorable combined genotype for litter size traits. These results identified favorable alleles and genotypes for litter size traits and suggested a potential selection scheme for litter size in Large White pigs.

SLA-11 mutations are associated with litter size traits in Large White and Chinese DIV pigs.

Litter size is an important economic traits in pigs. SLA-11 gene is a member of SLA (swine leukocyte antigen) complex. In our previous study, the SLA-11 gene was differentially expressed in PMSG-hCG stimulated preovulatory ovarian follicles of Chinese Taihu and Large White sows. Here, we identified two mutations (c.754-132 T > C and c.1421 + 38 T > C) in SLA-11 gene and analyzed the associations of two SNPs with litter size traits in Large White (n = 263) and DIV (n = 117) sows. The results showed that in Large White pigs, SLA-11 c.754-132 CC sows produced 0.74 and 0.87 more pigs per litter for TNB and NBA of all parities than did TT sows (p < .05); In DIV pigs, SLA-11 c.754-132 CC sows produced 1.17 more pigs per litter for TNB of all parities than did TC sows (p < .05). In Large White pigs, SLA-11 c.1421 + 38 CC sows produced 0.9 more pigs per litter for TNB of all parities than did TT sows (p < .05), while in DIV pigs SLA-11 c.1421 + 38 CC sows produced 0.84 and 0.7 less pigs per litter for TNB and NBA of all parities than did TT sows (p < .05). Our research indicated that SLA-11 mutations were potential molecular markers for improving the litter size traits in pigs.

The transcription factor ccaat/enhancer binding protein ß (C/EBPß) and miR-27a regulate the expression of porcine Dickkopf2 (DKK2).

Using Affymetrix porcine Gene-Chip analyses, we found that Dickkopf2 (DKK2), a WNT antagonist, is differentially expressed in pre-ovulatory follicles between Large White and Chinese Taihu sows. This study aims to identify the regulatory factors responsible for DKK2 expression. Deletion fragment and mutation analyses identified DKK2-D3 as the porcine DKK2 core promoter. There were four C/EBPß binding sites within the DKK2 core promoter. The C allele that results from a spontaneous alteration (DKK2 c.-1130 T > C) in the core promoter was associated with a higher total number born (TNB) and a higher number born alive (NBA) in all parities in a synthetic pig population. This was possibly the result of a change in C/EBPß binding ability, which was confirmed using chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assays (EMSA). Moreover, C/EBPß specifically bound to and activated the DKK2 promoter, as revealed by mutation analysis, overexpression and RNA interference (RNAi) experiments. We also confirmed that miR-27a is a negative regulator of the DKK2 gene using miR-27a overexpression and inhibition experiments and mutation analyses. RTCA xCELLigence experiments showed that miR-27a suppressed Chinese hamster ovary (CHO) cell proliferation by down-regulating DKK2 gene expression. Taken together, our findings suggest that C/EBPß and miR-27a control DKK2 transcription.