Article

Current Allergy and Asthma Reports

, Volume 5, Issue 1, pp 67-73

A genetic engineering strategy to eliminate peanut allergy

  • Hortense DodoAffiliated withFood Biotechnology Laboratory, Department of Food & Animal Sciences, Alabama A&M University
  • , Koffi KonanAffiliated withFood Biotechnology Laboratory, Department of Food & Animal Sciences, Alabama A&M University
  • , Olga ViquezAffiliated withFood Biotechnology Laboratory, Department of Food & Animal Sciences, Alabama A&M University

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Abstract

Peanut allergy is an IgE-mediated hypersensitivity reaction with an increasing prevalence worldwide. Despite its seriousness, to date, there is no cure. Genetic engineering strategies can provide a solution. The post-transcriptional gene silencing (PTGS) model can be used effectively to knock out the production of allergenic proteins in peanut by specific degradation of the endogenous target messenger RNA (mRNA). Ara h 2, the most potent peanut allergenic protein, was selected as a model to demonstrate the feasibility of this concept. Transgenic peanut plants were produced via microprojectile-mediated transformation of peanut embryos using a plasmid construct, which contains a fragment of the coding region of Ara h 2 linked to an enhanced CaMV 35S constitutive promoter. Molecular analyses, including polymerase chain reaction and Southern blots, confirmed the presence of the stable integration of the Ara h 2 transgene into the peanut genome. Northern hybridization showed the expression of the Ara h 2 transgene in all vegetative tissues of the mature transgenic peanut plants, indicating the stable expression of the truncated Ara h 2 transgene throughout the development of the plants. It is, therefore, reasonable to expect that the truncated Ara h 2 transgene transcripts will be synthesized in the seeds and will trigger the specific degradation of endogenous Ara h 2 mRNA. The next step will be to grow the transgenic peanut plants to full maturity for seed production and to determine the level of allergen Ara h 2.