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ARS Home » Midwest Area » West Lafayette, Indiana » Crop Production and Pest Control Research » Research » Publications at this Location » Publication #155824


item Wiangjun, Hathaithip
item Anderson, Joseph

Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/1/2004
Publication Date: 10/1/2004
Citation: Wiangjun, H., Anderson, J.M. 2004. The basis for Thinopyrum-derived resistance to Cereal Yellow Dwarf Virus. Phytopathology. 94:1102-1106.

Interpretive Summary: Cereal Yellow Dwarf Virus (CYDV) can cause significant yield loss in economically important cereal crops including wheat, barley, and oats. The absence of natural resistance in wheat to CYDV led to the incorporation of resistance from a related wheatgrass. However, little is know about the mechanism of this resistance. We have shown that this resistance does not stop CYDV replication but rather localizes the disease to the site where the plant was inoculated. This does not allow the virus to spread to the rest of the plant. These results will allow us and other scientists to identify the virus protein which the resistant plant must recognize to stop virus movement throughout the plant. Using this information it may be possible to develop wheat that has increased resistance to other important related viruses of wheat.

Technical Abstract: The incorporation of Thinopyrum intermedium-derived resistance gene(s) into improved wheat germplasm generated a wheat substitution line P29 whose 7D chromosome was replaced by Th. intermedium chromosome 7E. Resistance in P29 was previously proven to be highly effective to Cereal yellow dwarf virus (CYDV). The undetectable CYDV titer in P29 led many to conclude that resistance prevented the replication of CYDV. To determine if this resistance is due to a block in CYDV replication or movement we examined the inoculated leaf for replication and uninoculated leaves for systemic infection. CYDV subgenomic RNA, produced only during replication, was found within the inoculated portion of the leaves of P29 and Th. intermedium, which indicated that the viral replication was not effected. The absence of CYDV from the uninoculated, newly emerging leaves of inoculated P29 and Th. intermedium plants suggested the inhibition of viral systemic infection. Resistance could be overcome, resulting in a systemic spread of CYDV, if P29 was inoculated at the 1-leaf stage or younger with 50 to 100 viruliferous aphids per plant. As these infected P29 seedlings continued to grow, the resistance phenotype was recovered. However, when the number of aphids used in the inoculation was small, 7 to 10 viruliferous aphids per plant, the resistance was maintained across all the developmental stages tested. Our data indicated that Th. intermedium-derived resistance to CYDV was primarily dosage-dependent and was developmentally regulated if the amount of inoculum was large enough.