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>Journals >Veterinaria México >Year 2005, Issue 3

Riojas-Valdés VM, Canales-Zambrano JC, Gómez-de la Fuente JC, Dávalos-Aranda G, Hernández-Vidal G, Salinas-Meléndez JA
Allele frequency of porcine stress syndrome in Nuevo Leon by PCR-RFLP analysis
Vet Mex 2005; 36 (3)

Language: English/Spanish
References: 19
Page: 261-267
PDF: 337.00 Kb.

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Porcine stress syndrome (PSS), caused by a point mutation in the gene coding for the ryanodine receptor (locus ryr-1), is one of the problems the pork industry is facing today. PSS, also known as malignant hyperthermia, causes death in animals or lower meat product quality. These problems arise in the affected animals when they are under stressful conditions, such as during transportation. Currently, there are no data on the gene frequency of the condition in Nuevo Leon; however, anecdotal evidence points to a frequency similar to that of countries in which data do exist for the Landrace, Duroc, Large White and Hampshire breeds. In the present study a molecular biology technique was used to determine the genotype of animals for the syndrome, based on the polymerase chain reaction and the digestion of its products with a restriction enzyme (PCR-RFLP). A total of 77 animals were analyzed, of which 23 presented the recessive allele (29.9%); according to the genotype, 26% were carriers (N/n) and 3.9% were affected (n/n); the rest, 54 animals (70.1%), had a normal genotype (N/N). There was no significant difference in mutation frequency between males (33.4%) and females (26.3%), although there were more affected females than males (nn). Genotype frequencies found were 0.70 (54/77) for the dominant homozygote (NN), 0.26 (20/77) for the heterozygote (Nn) and 0.04 (3/77) for the recessive homozygote. Frequencies were 0.17 for the recessive allele (n) and 0.83 for the dominant one (N).

Key words: Porcine, Stress syndrome, Pcr-Rflp.


  1. MacLennan DH. The genetic basis of malignant hyperthermia. Trends Pharmacol Sci. 1992; 13:329-334.

  2. Ball SP, Johnson KJ. The Genetics of malignant hyperthermia. Med Genet 1993; 30:89-93.

  3. Otsu K, Khanna VK, Archibald A L, MacLennan DH. Cosegregation of porcine malignant hyperthermia and a probable casual mutation in the skeletal muscle ryanodine receptor gene in backcross families. Genomics 1991; 11:744-750.

  4. Rudolph JA, Spier J, Byrns G, Rojas CB, Bernoco D, Hoffman EP. Periodic Paralysis in Quarter Horses: a sodium channel mutation disseminated by selective breeding. Nat Genet. 1992; 2:144-147.

  5. Fujii J, Otsu K, Zorzato F, DeLeon S, Khanna VK, Weiler JE, et al., Identification of a mutation in porcine ryanodine receptor associated with malignant hypertermia. Science 1991; 253:448-451.

  6. Houde A, Pommier SA, Roy R. Detection of the ryanodine receptor mutation associated with malignant hyperthermia in purebred swine populations. Anim Sci 1993; 71:1414-1418.

  7. O’Brien PJ, Shen H, Cory CR, Zhang X. Use of a DNA-based test for the mutation associated with porcine stress syndrome (malignant hyperthermia) in 10,000 breeding swine. Am Vet Med Assoc 1993; 203:842-851.

  8. Brem G, Brening B. Use of molecular genetic diagnosis of malignant hyperthermic syndrome (MHS) in selection of pigs. Genetika 1993; 29:1009-1013.

  9. Watson JD, Hopkins NH, Roberts JW, Steitz JA, Weiner AM. Molecular biology of the gene. 4th ed. Menlo Park, California, U.S.A. Ed. Benjamin/Cummings Publishing Co. 1987; 668-670..

  10. Womack J E. Molecular genetics arrives on the farm. Nature 1992; 360:108-109.

  11. Oyamada H, Oguchi K, Saitoh N, Yamazawa T, Hirose K, Kawana Y, et al. Novel mutations in C-terminal channel region of the ryanodine receptor in malignant hyperthermia patients. Jpn J Pharmacol 2002; 88:159-166.

  12. Girard T, Urwyler A, Censier K, Mueller CR, Zorzato F, Treves S. Genotype-phenotype comparison of the Swiss malignant hyperthermia population. Hum Mutat 2001; 18: 357-358.

  13. Galli L, Orrico A, Cozzolino S, Pietrini V, Tegazzin V, Sorrentino V. Mutations in the RYR1 gene in Italian patients at risk for malignant hyperthermia: evidence for a cluster of novel mutations in the C-terminal region. Cell Calcium 2002; 32: 143-151.

  14. Brown RL, Pollock AN, Couchman KG, Hodges M, Hutchinson DO, Waaka R, et al. A novel ryanodine receptor mutation and genotype-phenotype correlation in a large malignant hyperthermia. New Zealand Maori pedigree. Hum Mol Genet 2000; 9: 1515-1524.

  15. Roberts MC, Mickelson JR, Patterson EE, Nelson TE, Armstrong PJ, Brunson DB, et al. Autosomal dominant canine malignant hyperthermia is caused by a mutation in the gene encoding the skeletal muscle calcium release channel (RYR1). Anesthesiology 2001; 95: 716-725.

  16. Ruffert H, Olthoff D, Deutrich C, Thamm B, Froster U. In vitro contracture test and gene typing in diagnosing malignant hyperthermia. Each as an appropriate complement to the other method. Anasthesist 2000; 49: 113-120.

  17. Maddock RJ, Bidner BS, Carr SN, McKeith FK, Berg EP, Savell JW. Creatine monohydrate supplementation and the quality of fresh pork in normal and halothane carrier pigs. J Anim Sci 2002; 80: 997-1004.

  18. Hamilton DN, Ellis M, Millar KD, McKeith FK, Parrett DF. The effect of the Halothane and Rendement Napole genes on carcass and meat quality characteristics of pigs. J Anim Sci 2000; 78: 2862-2867.

  19. Weaver RF, Hedrick PW. Genetics. Wm C. Brown Publishers, U.S.A. 1989.

>Journals >Veterinaria México >Year 2005, Issue 3

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