Expression of 3-OH trichothecene acetyltransferase in barley (Hordeum vulgare L.) and effects on deoxynivalenol

Fusarium head blight (FHB), caused primarily by Fusarium graminearum, has been the most destructive disease of barley (Hordeum vulgare L.) in the USA since the early 1990s, resulting in large economic losses for growers. The fungus produces the mycotoxin deoxynivalenol (DON), a protein synthesis inhibitor, which is harmful to humans and livestock. Chemically modifying DON could reduce DON accumulation in the grain. We introduced Tri101, which encodes a 3-OH trichothecene acetyltransferase that converts DON to a less toxic acetylated form, into the cultivar Conlon through particle bombardment of callus in an attempt to detoxify DON. Southern analyses confirmed six independent integrations of Tri101 into the barley genome. Northern, Western and trichothecene acetyltransferase activity analyses confirmed the inheritance and expression of Tri101 in the progenies of three independent transgenic lines. Greenhouse tests of T3 and T4 transgenic lines showed a reduction in DON concentration; however, field tests of T4 transgenic lines showed no reduction in DON accumulation. The field tests also showed the presence of somaclonal variation in the transgenic plants. The backcrossed transgenic lines were tested in the field and showed no reduction in DON accumulation. The backcrossed transgenic lines had reduced trichothecene acetyltransferase activity compared to the T4 lines and DON levels comparable to wild-type Conlon barley under field tests.