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Characterization of polymorphisms of transferrin receptor and their association with susceptibility to ETEC F4ab/ac in pigs
Author(s) -
Wang Y.,
Ren J.,
Lan L.,
Yan X.,
Huang X.,
Peng Q.,
Tang H.,
Zhang B.,
Ji H.,
Huang L.
Publication year - 2007
Publication title -
journal of animal breeding and genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.689
H-Index - 51
eISSN - 1439-0388
pISSN - 0931-2668
DOI - 10.1111/j.1439-0388.2007.00664.x
Subject(s) - biology , linkage disequilibrium , genetics , single nucleotide polymorphism , locus (genetics) , enterotoxigenic escherichia coli , genotype , snp , intron , exon , gene , escherichia coli , enterotoxin
Summary Diarrhoea caused by enterotoxigenic Escherichia coli (ETEC) expressing F4 (F4ab, F4ac and F4ad) fimbriae is a significant cause of mortality and morbidity in newborn and weaned pigs. The locus controlling susceptibility towards ETEC F4ab/ac has been mapped to SSC13q41, in which TFRC (transferrin receptor) was localized and considered as a positional candidate gene for ETEC F4ab/ac receptor. In this study, we determined susceptibility/resistance to ETEC F4ab/ac in a total of 755 F 2 animals from a White Duroc × Erhualian intercross using a microscopic enterocyte adhesion assay. We identified two TFRC polymorphisms (SNPs 591 A>G and 632 A>G) in a single exon after comparative sequencing analysis of 2371‐bp amplicons containing the complete coding region of TFRC using RNA of eight full‐sib F 2 animals with susceptible and resistant phenotypes. The intron sequences flanking the two exon polymorphisms were obtained, revealing an intron polymorphism (SNP 291 C>T). We genotyped the 19 founder animals of the White Duroc × Erhualian intercross for the identified polymorphisms, showing that only the 291 C>T polymorphism is a highly informative marker. We further genotyped all 59 F 1 and 755 F 2 animals for the 291 C>T polymorphism, and the association of this polymorphism with susceptibility/resistance to ETEC F4ab/ac in these F 2 animals was evaluated by the transmission disequilibrium test. The result showed that the 291 C>T polymorphism is not a causal mutation, however, has a significant linkage disequilibrium with the ETEC F4ab/ac, especially F4ac receptor locus.