Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/12/2008
Publication Date: 3/10/2009
Citation: Garvin, D.F., Stack, R.W., Hansen, J.M. 2009. Quantitative Trait Locus Mapping of Increased Fusarium Head Blight Susceptibility Associated with a Wild Emmer Wheat Chromosome. Phytopathology. 99(4):447-452. Interpretive Summary: Fusarium head blight (FHB) is a disease that has caused several billion dollars of damage to the U.S. wheat crop over the last 15 years alone. Plant breeders have introduced FHB resistance genes to reduce the damage caused by this disease; however, their effectiveness may in theory be reduced by "suppressor" genes, as has been observed for other wheat diseases. In this study, we sought to characterize the genetic basis of FHB resistance gene suppression associated with a particular chromosome of a wheat ancestor and to identify the chromosome location of the suppressor gene. Results of our genetic analyses found evidence for the presence of one FHB resistance suppressor gene on the chromosome being studied. This gene not only suppresses a known major FHB resistance gene located on another chromosome but also confers a significant increase in disease susceptibility. Molecular mapping studies revealed that this FHB resistance suppressor gene is located near the middle of the chromosome. These results provide firm evidence for the existence of genes that can suppress the effect of FHB resistance genes. This finding points to an alternative strategy for improving FHB resistance in wheat by eliminating suppressor genes at the same time as resistance genes are being introduced. By improving FHB resistance in wheat, crop yield and quality will be improved. This in turn will improve farm profits and food security.
Technical Abstract: Chromosome 2A of wild emmer (Triticum turgidum var. dicoccoides) line Israel A increases Fusarium head blight (FHB) severity when present in durum wheat (T. turgidum var. durum) cvc. Langdon (LDN), suggesting that FHB susceptibility genes are located on this chromosome. The goals of this study were to explore the genetics of increased FHB susceptibility conferred by this chromosome, to examine the interaction between chromosome 2A FHB susceptibility factors and a FHB resistance QTL on Israel A chromosome 3A, and to identify regions of chromosome 2A that increase FHB susceptibility. Disease evaluations of LDN, the Langdon-Israel A chromosome 2A substitution line LDN(DIC-2A), and LDN x LDN(DIC-2A) F1 hybrids revealed that FHB susceptibility associated with chromosome 2A is additive, in contrast to FHB resistance conferred by the QTL Qfhs.ndsu-3AS, which acted in a dominant fashion. In F1 hybrids between LDN(DIC-2A) and LDN(DIC-3A) which harbors Qfhs.ndsu-3AS, FHB severity was similar to the midparent mean, indicating that Israel A chromosome 2A partially suppresses the action of Qfhs.ndsu-3AS. Disease evaluations of an F2 population from the cross LDN(DIC-2A) x LDN(DIC-3A) supported this finding. A recombinant inbred chromosome line (RICL) population from the cross LDN x LDN(DIC-2A) was used for QTL analysis of FHB susceptibility. A region of the long arm of chromosome A was identified with increased FHB susceptibility in three separate FHB evaluations. The single best SSR marker in each evaluation accounted for between 21% and 26% of the variation for FHB susceptibility, depending on the evaluation, with the susceptible allele coming from Israel A. These results indicate that genes that suppress FHB resistance are present in the genus Triticum, and that elimination of such genes may provide an avenue for enhancing the effectiveness of FHB resistance genes.