Open Access Short Report

Characterisation of five candidate genes within the ETEC F4ab/ac candidate region in pigs

Mette Jacobsen1, Susanna Cirera1, David Joller2, Gloria Esteso3, Steffen S Kracht1, Inger Edfors4, Christian Bendixen5, Alan L Archibald6, Peter Vogeli2, Stefan Neuenschwander2, Hans U Bertschinger2, Antonio Rampoldi2, Leif Andersson7, Merete Fredholm1 and Claus B Jørgensen1*

Author Affiliations

1 Department of Basic Animal and Veterinary Sciences, University of Copenhagen, 1870 Frederiksberg, Denmark

2 Institute of Agricultural Sciences, ETH Zurich, 8092 Zurich, Switzerland

3 Genomica y Mejora Animal, Departamento de Genética, Universidad de Córdoba, Campus de Rabanales, 14071, Córdoba, Spain

4 School of Natural Sciences, Linnaeus University, 391 82 Kalmar, Sweden

5 Department of Genetics and Biotechnology, Aarhus University, 8830 Tjele, Denmark

6 Division of Genetics and Genomics, The Roslin Institute and R(D)SVS, University of Edinburgh, Roslin, Midlothian EH25 9PS, UK

7 Department of Medical Biochemistry and Microbiology, Uppsala University, 751 23 Uppsala, Sweden

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BMC Research Notes 2011, 4:225  doi:10.1186/1756-0500-4-225

Published: 30 June 2011



Enterotoxigenic Escherichia coli (ETEC) that express the F4ab and F4ac fimbriae is a major contributor to diarrhoea outbreaks in the pig breeding industry, infecting both newborn and weaned piglets. Some pigs are resistant to this infection, and susceptibility is inherited as a simple dominant Mendelian trait. Indentifying the genetics behind this trait will greatly benefit pig welfare as well as the pig breeding industry by providing an opportunity to select against genetically susceptible animals, thereby reducing the number of diarrhoea outbreaks. The trait has recently been mapped by haplotype sharing to a 2.5 Mb region on pig chromosome 13, a region containing 18 annotated genes.


The coding regions of five candidate genes for susceptibility to ETEC F4ab/ac infection (TFRC, ACK1, MUC20, MUC4 and KIAA0226), all located in the 2.5 Mb region, were investigated for the presence of possible causative mutations. A total of 34 polymorphisms were identified in either coding regions or their flanking introns. The genotyping data for two of those were found to perfectly match the genotypes at the ETEC F4ab/ac locus, a G to C polymorphism in intron 11 of TFRC and a C to T silent polymorphism in exon 22 of KIAA0226. Transcriptional profiles of the five genes were investigated in a porcine tissue panel including various intestinal tissues. All five genes were expressed in intestinal tissues at different levels but none of the genes were found differentially expressed between ETEC F4ab/ac resistant and ETEC F4ab/ac susceptible animals in any of the tested tissues.


None of the identified polymorphisms are obvious causative mutations for ETEC F4ab/ac susceptibility, as they have no impact on the level of the overall mRNA expression nor predicted to influence the composition of the amino acids composition. However, we cannot exclude that the five tested genes are bona fide candidate genes for susceptibility to ETEC F4ab/ac infection since the identified polymorphism might affect the translational apparatus, alternative splice forms may exist and post translational mechanisms might contribute to disease susceptibility.