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ARS Home » Midwest Area » St. Paul, Minnesota » Plant Science Research » Research » Publications at this Location » Publication #262030
Title: A novel genome mutation in wheat increases Fusarium Head Blight resistance

Author
item Garvin, David
item PORTER, HEDERA - University Of Minnesota
item Blankenheim, Zachary
item Chao, Shiaoman
item DILL-MACKY, RUTH - University Of Minnesota

Submitted to: National Fusarium Head Blight Forum
Publication Type: Abstract Only
Publication Acceptance Date: 11/10/2010
Publication Date: 12/7/2010
Citation: Garvin, D.F., Porter, H., Blankenheim, Z., Chao, S., Dill-Macky, R. 2010. A novel genome mutation in wheat increases Fusarium Head Blight resistance [abstract]. In: Proceedings of the 2010 National Fusarium Head Blight Forum, December 7-9, 2010, Milwaukee, Wisconsin. p. 142.

Interpretive Summary:

Technical Abstract: We sought to validate an FHB resistance QTL reported to be on chromosome 2A in the soft red winter wheat cultivar Freedom by introducing it into the highly susceptible rapid maturing dwarf wheat Apogee. Marker-assisted backcrossing with an SSR marker reported to be associated with this QTL was undertaken. One backcross four-derived Apogee near-isogenic line (NIL), designated A30, exhibited improved type II FHB resistance. Other independently derived NILs harboring the introgressed Freedom SSR marker did not exhibit improved FHB resistance, suggesting that the FHB resistance of A30 could be due to the introgression of an unlinked major FHB resistance QTL from Freedom. A project was undertaken to identify marker loci for this putative new FHB resistance QTL. Ninety F2:3 families derived from the cross A30 x Apogee were evaluated for type II FHB resistance in two greenhouse evaluations. SSR marker polymorphisms between A30 and an FHB susceptible sib line, A31, were identified to provide targets for mapping the putative new QTL in the A30 x Apogee population. Sampling of markers in major intervals of A30 deriving from Freedom did not reveal an association to FHB resistance in the mapping population. However, when SSR markers present in A31 and Apogee, but null in A30, were examined, a significant relationship with FHB resistance was detected, with a positive effect associated with the null allele state. On average, F2:3 families homozygous for the null alleles were approximately 50% more resistant than Apogee in the greenhouse evaluations. Aneuploid analysis revealed the null alleles to be associated with chromosome arm 3DL. Evaluation of other markers on this chromosome arm identified a series of null markers in A30 located in bin 3 of the Chinese Spring segmental deletion lines. Interestingly, Freedom is not null for these SSR markers. We conclude that during the course of our backcrossing efforts between Apogee and Freedom, a segment of the terminal end of chromosome arm 3DL of Apogee was deleted. Deletion of this chromosome segment has a significant positive effect on type II FHB resistance. The gain of resistance associated with the loss of a chromosome segment suggests that the region contains either a suppressor of FHB resistance or a gene that promotes pathogenicity of F. graminearum. We are now examining whether this effect occurs in other genetic backgrounds.