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BMC Genet. 2014 Oct 3;15:103. doi: 10.1186/s12863-014-0103-x.

Variation in 12 porcine genes involved in the carbohydrate moiety assembly of glycosphingolipids does not account for differential binding of F4 Escherichia coli and their fimbriae.

Author information

1
Laboratory of Animal Genetics, Faculty of Veterinary Medicine, Ghent University, Heidestraat 19, B-9820, Merelbeke, Belgium. Tiphanie.Goetstouwers@Ugent.be.
2
Laboratory of Animal Genetics, Faculty of Veterinary Medicine, Ghent University, Heidestraat 19, B-9820, Merelbeke, Belgium. Mario.Vanpouke@Ugent.be.
3
Laboratory of Immunology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820, Merelbeke, Belgium. Anndelies.Coddens@telenet.be.
4
Laboratory of Immunology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820, Merelbeke, Belgium. Nguyen.VanUt@UGent.be.
5
Laboratory of Immunology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820, Merelbeke, Belgium. Vesna.Melkebeek@Ugent.be.
6
Laboratory of Pharmaceutical Biotechnology, Faculty of Pharmaceutical Sciences, Ghent University, Harelbekestraat 72, 9000, Ghent, Belgium. Dieter.Deforce@Ugent.be.
7
Laboratory of Immunology, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, 9820, Merelbeke, Belgium. Eric.Cox@Ugent.be.
8
Laboratory of Animal Genetics, Faculty of Veterinary Medicine, Ghent University, Heidestraat 19, B-9820, Merelbeke, Belgium. Luc.Peelman@Ugent.be.

Abstract

BACKGROUND:

Glycosphingolipids (GSLs) are important membrane components composed of a carbohydrate structure attached to a hydrophobic ceramide. They can serve as specific membrane receptors for microbes and microbial products, such as F4 Escherichia coli (F4 ETEC) and isolated F4 fimbriae. The aim of this study was to investigate the hypothesis that variation in genes involved in the assembly of the F4 binding carbohydrate moiety of GSLs (i.e. ARSA, B4GALT6, GAL3ST1, GALC, GBA, GLA, GLB1, GLB1L, NEU1, NEU2, UGCG, UGT8) could account for differential binding of F4 ETEC and their fimbriae.

RESULTS:

RT-PCR could not reveal any differential expression of the 12 genes in the jejunum of F4 receptor-positive (F4R(+)) and F4 receptor-negative (F4R(-)) pigs. Sequencing the complete open reading frame of the 11 expressed genes (NEU2 was not expressed) identified 72 mutations. Although some of them might have a structural effect, none of them could be associated with a F4R phenotype.

CONCLUSION:

We conclude that no regulatory or structural variation in any of the investigated genes is responsible for the genetic susceptibility of pigs towards F4 ETEC.

PMID:
25277275
PMCID:
PMC4189734
DOI:
10.1186/s12863-014-0103-x
[Indexed for MEDLINE]
Free PMC Article

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