Genetic variation at the alpha-1-fucosyltransferase (FUT1) gene in Asian wild boar and Chinese and Western commercial pig breeds

被引:72
作者
Bao, W. B. [1 ]
Wu, S. L. [1 ]
Musa, H. H. [1 ]
Zhu, G. Q. [2 ]
Chen, G. H. [1 ]
机构
[1] Yangzhou Univ, Coll Anim Sci & Technol, Yangzhou 225009, Peoples R China
[2] Yangzhou Univ, Coll Vet Med, Yangzhou 225009, Peoples R China
关键词
Alpha-1-fucosyltransferase (FUT1) gene; ETEC F18; Piglet;
D O I
10.1111/j.1439-0388.2008.00722.x
中图分类号
S8 [畜牧、 动物医学、狩猎、蚕、蜂];
学科分类号
0905 ;
摘要
Escherichia coli F18 bacteria producing enterotoxins and/or shigatoxin (ETEC/STEC) are main pathogens that cause oedema disease and postweaning diarrhoea in piglets, and alpha-1-fucosyltransferase (FUT1) gene has been identified as a candidate gene for controlling the expression of ETEC F18 receptor. The genetic variations at nucleotide position 307 in open reading frame of FUT1 gene in one wild boar breed and 20 western commercial and Chinese native pig breeds were investigated by polymerase chain reaction-restriction fragment length polymorphism. The results showed that the genetic polymorphisms of the FUT1 locus were only detected in western pig breeds and the Chinese Taihu (including Meishan pig, Fengjing pig and Erhualian pig), Huai and Lingao pig breeds; only Duroc and Pietrain possessed the resistant AA genotype, while the wild boar and other Chinese pig breeds only presented the susceptible genotype GG. The results indicated that Chinese native pig breeds lack genetic factors providing resistance to ETEC F18 bacteria. The resistant allele to ETEC F18 might originate from European wild boar. It was inferred that oedema and postweaning diarrhoea caused by ETEC F18 have close relationship with the growth rate, which can explain why on the contrary Chinese native pig breeds have stronger resistance to oedema and postweaning diarrhoea in piglets compared with western pig breeds. © 2008 The Authors.
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页码:427 / 430
页数:4
相关论文
共 15 条
[1]  
Giuffra E., Kiias J.M.H., Armager V., Carlborg O., Jeon J.T., Andersson L., The origin of the domestic pig - Independent domestication and subsequent introgression, Genetics, 154, pp. 1785-1791, (2000)
[2]  
He W.M., Jiang Y.F., Luo W.H., Huang J.W., Zhang Y.J., Li M.Q., Liu B.Z., Pathogenic diagnosis and epidemiological investigation on edema disease of pigs, Acta. Agri. Boreali-occidentalis Sinica, 10, pp. 1-5, (2001)
[3]  
Hong X.H., Zhu R.Z., Pang Q.H., Li H.Q., Gao S., Yang H.W., Ding Y.L., Prevalence of virulence factors of Escherichia coli strains isolated from swine edema disease and its epidemiology in Hai'an, Jilin. Anim. Sci. Vet. Med., 3, pp. 6-7, (2005)
[4]  
Imberechts H., De Greve H., Schlicker C., Bouchet H., Pohl P., Charlier G., Bertschinger H., Wild P., Vandekerckhove J., Van Damme J., Characterization of F107 fimbriae of Escherichia coli 107/86 which causes oedema disease in pigs and nucleotide sequence of F107 major fimbrial subunit gene, fedA, Infect. Immun., 60, pp. 1963-1971, (1992)
[5]  
Jiang X.L., Diagnosis of edema disease in piglets, Gansu. Anim. Sci. Vet. Med., 31, pp. 24-25, (2001)
[6]  
Klukowska J., Urbaniak B., Switonski M., High frequency of M307<sup>A</sup> mutation at FUT1 locus, causing resistance to oedema disease, in an autochthonous polish pig breed, the Zlotnicka spotted, J. Anim. Breed. Genet., 116, pp. 519-524, (1999)
[7]  
Leng C.Y., Su D.H., Prevention and cure of edema disease in piglets, J. Anim. Sci. Vet. Med., 25, pp. 67-68, (2006)
[8]  
Meijerink E., Fries R., Vogeli P., Masabanda J., Wigger G., Stricker C., Neuenschwander S., Bertschinger H.U., Stranzinger G., Two α(1,2)fucosyltransferase genes on porcine chromosome 6q <sup>11</sup> are closely linked to the blood group inhibitor (S) and Escherichia coli F18 receptor (ECF18R) loci, Mamm. Genome, 8, pp. 736-741, (1997)
[9]  
Sambrook J., Russell D.W., Molecular Cloning: A Laboratory Manual., (2001)
[10]  
Shi Q.S., Xie X.M., Liu X.C., Huang S.Q., He C.Q., Experimental results on enterotoxigenic E. coli F18 receptor genotypes, Hereditas (Beijing), 24, pp. 656-658, (2002)