SummaryAlthough several wheat genes differentially expressed during the Russian wheat aphid resistance response have recently been identified, their requirement for and specific role in resistance remain unclear. Progress in wheat-aphid interaction research is hampered by inadequate collections of mutant germplasm and difficulty in transforming hexaploid wheat. Virus-induced gene silencing (VIGS) technology is emerging as a viable reverse genetics approach in cereal crops. However, the potential of VIGS for determining aphid defence gene function in wheat has not been evaluated. We report on the use of recombinant barley stripe mosaic virus (BSMV) to target and silence a WRKY53 transcription factor and an inducible phenylalanine ammonia-lyase (PAL) gene, both predicted to contribute to aphid defence in a genetically resistant wheat line. After inoculating resistant wheat with the VIGS constructs, transcript abundance was reduced to levels similar to that observed in susceptible wheat. Notably, the level of PAL expression was also suppressed by the WKRY53 construct, suggesting that these genes operate in the same defence response network. Both knockdowns exhibited a susceptible phenotype upon aphid infestation, and aphids feeding on silenced plants exhibited a significant increase in fitness compared to aphids feeding on control plants. Altered plant phenotype and changes in aphid behaviour after silencing imply that WKRY53 and PAL play key roles in generating a successful resistance response. This study is the first report on the successful use of VIGS to investigate genes involved in wheat-insect interactions.

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High-temperature, adult-plant (HTAP) resistance to stripe rust (Puccinia striiformis West) in wheat (Triticum aestivum L. em Tbell) bas remained durable for at least 30 yr in tbe USA. Tbe expression of HTAP resistance to stripe rust in six crosses of winter wheat was evaluated using F 6 populations at Pullman, WAin 1986 and F 7 populations at three environmentally different locations (Pullman, Mt. Vernon, and Walla Walla, WA) in 1987. Resistant families could not be differentiated at Pullman in 1986 and Walla Walla in 1987 because unfavorable weather delayed tbe development of rust. Differences in rust intensity for families within eacb cross could be determined at Mt. Vernon and Pullman in 1987. Distributions of disease intensities for families of eacb cross were significantly different between tbe two locations. Negative correlations between three yield components (kernel number, kernel weight, and spike weight) and rust intensity at several plant growth stages were bigb when infection was early and rust intensity was severe, but were not significant wben infection was late and rust intensities were moderate or low. Early rust development negatively affected kernel number. At Mt. Vernon, tbe plant growth stages at wbicb yield components were most bigbly correlated witb rust intensities varied depending on tbe cross. Most yield components were highly correlated with disease intensity at beading and milk stages.Tbe environment at Pullman was appropriate and possibly better suited for selection of moderate or bigber levels of HTAP resistance wbicb

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