Genetic Variations of TAP1 Gene Exon 3 Affects Gene Expression and Escherichia coli F18 Resistance in Piglets

Abstract

Firstly, our research group identified Sutai pigs’ phenotypes that exhibited extreme resistance and susceptibility to the Escherichia coli F18 respectively, and then eight ETEC (Enterotoxigenic Escherichia coli) F18-resistant piglets and eight ETEC F18-sensitive piglets were selected. Then, the TAP1 (Transporter associated with antigen processing) mRNA relative expression levels were analyzed in 11 tissues of the resistant and susceptible phenotypes. Simultaneously, we detected the genetic variations in exon 3 of the TAP1 gene and evaluated the TAP1 mRNA expression levels among the different genotype pigs to study the effects of the genetic variation on gene expression, and the E. coli F18 resistance. The results revealed higher expression levels in the resistant genotypes than that in the susceptible genotypes in 11 tissues, with significant differences in the spleen, lymph node, lung, thymus, duodenum and jejunum. Furthermore, a G729A mutation was identified in the TAP1 gene exon 3, and this mutation deviates from Hardy-Weinberg equilibrium (p < 0.01). The TAP1 mRNA levels in GG genotype were significantly higher than that in the other two genotypes, with significant differences in the liver, lung, kidney, thymus, lymph node, duodenum and jejunum tissues. We speculated that high expression of the TAP1 gene might confer resistance against the E. coli F18, the G729A mutation had a significant effect on the mRNA expression, and individuals with the GG genotype possessed a stronger ability to resist the E. coli F18 infection.

Analysis of polymorphisms in the FUT1 and TAP1 genes and their influence on immune performance in Pudong White pigs

“…TAP1 plays a significant role in immune responses because of its increased expression level after infection by viruses and bacteria. Zhao et al (2014) analyzed TAP1 mRNA relative expression levels in 11 tissues from resistant and susceptible phenotypes, and found that the G729A mutation of TAP1 had a significant effect on TAP1 mRNA expression, with high expression possibly conferring resistance against E. coli F18, which confirms that the TAP1 gene plays an important role in E. coli F18 resistance (Wang et al, 2014). These results are also in agreement with Bao et al (2012).…”

“…The primer pair used for FUT1 ) amplification was F: 5'-CTTCCTGAACGTCATCAAGACC-3' and R: 5'-CTTCAGCCAGGGCTCCTTTAAG-3' (Sangon, Shanghai, China). The primer pair for TAP1 exon 3 (Sun et al, 2012;Zhao et al, 2014) was F: 5'-GAAATGTGGATAAGAGCA-3' and R: 5'-AAACAGACGGATAATGAAAGAGG-3' (Sangon). Amplification reactions were carried out on 80 to 150 ng genomic DNA in a 50 μL reaction volume containing 48 μL compound pfu PCR buffer (final concentration 1X buffer, 2 mM MgCl 2 , 10 mM each dNTP, 25 μM each primer, and 5 U pfu polymerase; TaKaRa, Dalian, China).…”

Animal EnterotoxigenicEscherichia coli

“…This polybasic loop was proposed to benefit particularly the intestinal binding of F18-ETEC to pig intestines, in the absence of inhibitory milk glycans that follows weaning (210). Several investigators in China detected that the homozygous resistance genotype occurred only in certain western breeds and associated with genotypes for other forms of resistance (211–214). …”

Evidence-Based Approaches for Determining Effective Target Antigens to Develop Vaccines against Post-Weaning Diarrhea Caused by Enterotoxigenic Escherichia coli in Pigs: A Systematic Review and Network Meta-Analysis

“…Single nucleotide polymorphisms (SNPs) localized on alpha (1,2)-fucosyltransferase (FUT1) and bactericidal/permeability-increasing protein (BPI) genes are responsible for swine F18-ETEC susceptibility [ 10 , 11 , 12 ], while the porcine susceptibility or resistance to F4ac-ETEC is controlled by the Mucin4 (MUC4) and Mucin13 (MUC13) genes [ 13 , 14 , 15 ]. Genetically, some piglets lack the fimbriae receptor genes, and thus may be resistant to ETEC infections [ 1 , 16 ]. The presence or absence of intestinal receptors for ETEC attachment and colonization determines the probability of the piglets developing PWD [ 8 , 17 ].…”