|Liu, Z - PLNT PATH, NDSU, FARGO ND|
|Meinhardt, S - BIOCHEM, NDSU, FARGO, ND|
|Ali, S - PLNT PATH, NDSU, FARGO ND|
|Rasmussen, J - PLNT PATH, NDSU, FARGO ND|
Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 11, 2004
Publication Date: September 15, 2004
Citation: Liu, Z.H., Friesen, T.L., Rasmussen, J.B., Ali, S., Meinhardt, S.W., Faris, J.D. 2004. Qtl analysis and mapping of seedling resistance to stagonospora nodorum leaf blotch in wheat.. Phytopathology. Vol.94:1061-1067. Interpretive Summary: Stagonospora nodorum leaf blotch (SNB) is an economically important foliar disease in the major wheat growing areas of the world. Utilization of host resistance is considered to be the most important and preferred method to control disease. The S. nodorum isolate Sn2000 produces a protein toxin that causes necrosis in sensitive wheat lines. Insensitivity to the toxin is controlled by a single gene designated snn1 on the short arm of chromosome 1B. In this research, we showed that snn1 is a major factor for resistance to the disease and that the toxin is a major virulence factor for the fungus. In addition to the toxin insensitivity gene, several additional genes with minor effects for resistance were identified. The molecular markers linked to these genes will be useful for incorporating the resistance genes into adapted germplasm.
Technical Abstract: Stagonospora nodorum leaf blotch (SNB) is an economically important foliar disease in the major wheat growing areas of the world. Utilization of host resistance is considered to be the most important and preferred method to control disease. In related work, we identified a host-selective toxin (SnTox1) produced by the isolate Sn2000 and mapped the gene (Snn1) conditioning sensitivity to chromosome 1BS. Here, we screened the ITMI mapping population and cytogenetic stocks, including nullisomic-tetrasomic (NT) lines and CS-Triticum dicoccoides (CS-DIC) substitution lines, with isolate Sn2000 to identify QTLs associated with resistance to SNB. QTL analysis revealed that the toxin sensitivity locus (Snn1) underlies a major QTL and explained 58.3, 47.7, and 27 percent of the phenotypic variation for 5, 7, and 10-day readings, respectively. This 1BS QTL, a minor QTL on chromosome 4BL, and an interaction between Snn1 and a marker on chromosome 2B explained as much as 66 percent of the total phenotypic variation. An additional QTL on chromosome 7BL was identified for the 10-day readings. Toxin sensitivity was highly correlated with chlorotic flecking on the leaves, which occurred in the early stages of disease development. N1BT1D and CS-DIC 1B were absent of chlorotic flecking and less susceptible to the fungus. These results in combination with the decreased effects of the 1BS QTL from 5 to 7 to 10 days indicate that the toxin is a major virulence factor, and is most effective in the early stages of the interaction.