Author
Garvin, David | |
PORTER, HEDERA - University Of Minnesota | |
Blankenheim, Zachary | |
Chao, Shiaoman | |
DILL-MACKY, RUTH - University Of Minnesota |
Submitted to: Genome
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 9/21/2015 Publication Date: 10/15/2015 Citation: Garvin, D.F., Porter, H., Blankenheim, Z., Chao, S., Dill-Macky, R. 2015. A spontaneous segmental deletion from chromosome arm 3DL enhances Fusarium head blight resistance in wheat. Genome. 58(11):479-488. Interpretive Summary: Fusarium head blight is a disease that has caused several billion dollars of damage to the U.S. wheat crop over the last two decades. Plant breeders have tried to introduce Fusarium head blight resistance genes to reduce the damage caused by this disease; however, their effectiveness varies and this may be due to genes that interfere with their functionality, as has been observed for some other wheat diseases. In this study, we sought to characterize the genetic basis of Fusarium head blight resistance associated with what was believed to be a new wheat Fusarium head blight resistance gene. Results of our analyses found evidence that the improved resistance we observed was actually due to a spontaneous mutation that eliminates a segment of a wheat chromosome. Thus, the resistance derives not from the addition of a new gene, but rather to the elimination of one or more genes. This result provides evidence for the potential existence of genes in wheat that act as susceptibility factors for the fungal pathogen that causes Fusarium head blight, a phenomenon observed for many other plant diseases. This finding points to an alternative strategy for improving Fusarium head blight resistance in wheat by eliminating such susceptibility genes. By improving Fusarium head blight resistance in wheat, crop yield and quality will be improved. This in turn will improve farm gate profits and food security. Technical Abstract: Much effort has been directed at identifying sources of resistance to Fusarium head blight (FHB) in wheat. We sought to identify molecular markers for what we hypothesized was a new major FHB resistance locus originating from the wheat cultivar 'Freedom' and introgressed into the susceptible wheat cultivar 'USU-Apogee.' An F2:3 mapping population from a cross between Apogee and A30, its BC4- near-isoline exhibiting improved FHB resistance, was evaluated for resistance. The distribution of FHB resistance in the population approximated a 1:3 moderately resistant:moderately susceptible+susceptible ratio. Separate disease evaluations established that A30 accumulated less deoxynivalenol and yielded a greater proportion of sound grain than Apogee. Molecular mapping revealed that the FHB resistance of A30 is associated with molecular markers on chromosome arm 3DL that exhibit a null phenotype in A30 but are present in both Apogee and Freedom, indicating a spontaneous deletion occurred during the development of A30. Aneuploid analysis revealed that the size of the deleted segment is approximately 19% of the arm's length. Our results suggest that the deleted interval of chromosome arm 3DL in Apogee may harbor FHB susceptibility genes that promote disease spread in infected spikes, and that their elimination increases FHB resistance in a novel manner. |