Open AccessIncreased field resistance to Tilletia caries provided by a specific antifungal virus gene in genetically engineered wheat
Author(s) -
Schlaich Thomas,
Urbaniak Bartosz M.,
Malgras Nicole,
Ehler Elisabeth,
Birrer Christof,
Meier Lukas,
Sautter Christof
Publication year - 2006
Publication title -
plant biotechnology journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.525
H-Index - 115
eISSN - 1467-7652
pISSN - 1467-7644
DOI - 10.1111/j.1467-7652.2005.00158.x
Subject(s) - biology , transgene , smut , gene , inoculation , spore , genetically modified crops , genetically modified organism , microbiology and biotechnology , botany , horticulture , genetics
Summary The field performance of a viral gene in two Swiss wheat ( Triticum aestivum ) varieties showed 10% increased fungal resistance against Tilletia caries (stinking smut). To the best of our knowledge, this is the first report of improved resistance against any fungus in the field achieved by genetic engineering in wheat. The genetically modified wheat lines previously showed a c . 30% decrease in symptoms of T. caries in the glasshouse (Clausen, M., Kräuter, R., Schachermayr, G., Potrykus, I. and Sautter, C. (2000) Antifungal activity of a virally encoded gene in transgenic wheat. Nat. Biotechnol . 18 , 446–449), depending on the fungal strain inoculated. A glasshouse experiment run in parallel to the field test, and using the same collection of T. caries , gave the same results. In a dose–response experiment with isolated fungal strains, in which the infection pressure was varied via the spore concentration, the transgene behaved as a quantitative resistance gene and shifted the S‐shaped dose–response curve towards higher resistance. The transgene was shown to be highly specific for fungi of the order Ustilaginales. Tests of the transgene using cell cultures of eukaryotes, including hamster and human, showed no significant side‐effects with respect to biosafety. Endogenous pathogen‐related genes were also activated on fungal infection in the presence of the kp4 transgene.