Abstract
Recent research confirms that genetic liability to halothane reaction and porcine stress syndrome (PSS) is largely controlled by a single locus (HAL), with evidence of genetic and maternal effects on expression. It now appears that the gene causing halothane reaction (n) may not be fully recessive, either for halothane sensitivity or meat quality. Nevertheless annual benefits from producing a heterozygous (Nn) slaughter generation in the UK could reach £20 million. The incidence of halothane reaction in European Landrace strains ranges from 1 to 100%. Continued selection for improved lean content is expected to increase the frequency of the halothane gene (n). Phenotypic halothane screening programmes would then only serve to hold gene frequencies at intermediate equilibria. A long term case therefore exists for eliminating the gene from maternal lines. Elimination by test-mating to positive homozygotes (nn) may prove prohibitively expensive. One option might be to await cheaper and more efficient methods of genotyping before attempting elimination. Immediate priorities for research are to devise new methods of genotyping, and to determine the net economic advantage of the heterozygote (Nn).
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