Submitted to: Theoretical and Applied Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/24/2011
Publication Date: 4/28/2011
Citation: Chung, C., Poland, J.A., Kump, K., Benson, J., Longfellow, J.M., Walsh, E.K., Balint Kurti, P.J., Nelson, R.J. 2011. Targeted discovery of quantitative trait loci for resistance to northern leaf blight and other diseases of maize. Theoretical and Applied Genetics. 123:307-326. Interpretive Summary: One way of looking for genes or loci which affect important traits that vary continuously (like height or yield) is to examine families where only a small percentage (say less than 10%) of the genome is varying (or segregating). IN these so-called heterozygous inbred families (HIFs) most of the genome is held constant so that effect of the variable part on the trait in question is more easily assessed. We have used HIFs to find loci conferring resistance to northern leaf blight of maize. We confirmed that the loci detected really do confirm resistance and have shown that some of them confer resistance to additional diseases.
Technical Abstract: To capture diverse alleles at a set of loci associated with disease resistance in maize, heterogeneous inbred family (HIF) analysis was applied for targeted QTL mapping and near-isogenic line (NIL) development. Tropical maize lines CML52 and DK888 were chosen as donors of alleles based on their known resistance to multiple diseases. Chromosomal regions (“bins”; n = 39) associated with multiple disease resistance (MDR) were targeted based on a consensus map of disease QTLs in maize. We generated HIFs segregating for the targeted loci but isogenic at ~97 % of the genome. To test the hypothesis that CML52 and DK888 alleles at MDR hotspots condition broad-spectrum resistance, HIFs and derived NILs were tested for resistance to northern leaf blight (NLB), southern leaf blight (SLB), gray leaf spot (GLS), anthracnose leaf blight (ALB), anthracnose stalk rot (ASR), common rust, common smut, and Stewart’s wilt. Four NLB QTLs, two ASR QTLs, and one Stewart’s wilt QTL were identified. In parallel, a population of 196 recombinant inbred lines (RILs) derived from B73 x CML52 was evaluated for resistance to NLB, GLS, SLB and ASR. The QTLs mapped (four for NLB, five for SLB, two for GLS and two for ASR) mostly corresponded to those found using the NILs. Combining HIF- and RIL-based analyses, we discovered two disease QTLs at which CML52 alleles were favorable for more than one disease. A QTL in bin 1.06-1.07 conferred resistance to NLB and Stewart’s wilt; and a QTL in 6.05 conferred resistance to NLB and ASR.