|CHUNG, CHIA-LIN - Cornell University - New York|
|LONGFELLOW, JOY - Cornell University - New York|
|WALSH, ELLIE - Cornell University - New York|
|KERDIEH, ZURA - West Virginia State University|
|VAN ESBROEK, GEORGE - North Carolina State University|
|NELSON, REBECCA - Cornell University - New York|
Submitted to: BMC Plant Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/8/2010
Publication Date: 6/8/2010
Citation: Chung, C., Longfellow, J.M., Walsh, E.K., Kerdieh, Z., Van Esbroek, G., Balint Kurti, P.J., Nelson, R.J. 2010. Resistance loci affecting distinct stages of fungal pathogenesis in maize: use of introgression lines for QTL mapping and characterization. Biomed Central (BMC) Plant Biology. 10:103.
Interpretive Summary: We do not have a good idea of the range of mechanism by which plants resist disease. Here we have identified two genomic regions from the maize line Tx303 that, when introduced into another maize line, B73, alter that line’s resistance to the fungal disease northern leaf blight. We show that one of these regions reduced the ability of the fungus to penetrate (get into) the leaf, while the other somehow impairs growth of the fungus after it has entered the leaf. We also show that these regions confer resistance to other fungal and bacterial diseases.
Technical Abstract: Background: Studies on host-pathogen interactions in a range of pathosystems have revealed an array of mechanisms by which plants reduce the efficiency of pathogenesis. While R-gene mediated resistance confers highly effective defense responses against pathogen invasion, quantitative resistance is associated with intermediate levels of resistance that reduces disease progress. To relate specific loci with effects on distinct stages of fungal pathogenesis, a set of maize introgression lines was used for mapping and characterization of quantitative trait loci (QTL) conditioning resistance to Setosphaeria turcica, the causal agent of northern leaf blight (NLB). To better understand the nature of quantitative resistance, the identified QTL were further tested for three secondary hypotheses: (1) that disease QTL differ by host developmental stage; (2) that their performance changes across environments ; and (3) that they condition broad-spectrum resistance. Results: Among a set of 82 introgression lines, seven lines were confirmed as more resistant or susceptible than B73. Two NLB QTL were validated in BC4F2 segregating populations and advanced introgression lines. These loci, designated qNLB1.02B73 (the B73 allele at bin 1.02) and qNLB1.06Tx303 (the Tx303 allele at bin 1.06), were investigated in detail by evaluating the introgression lines with a series of macroscopic and microscopic disease components targeting different stages of NLB development. Repeated greenhouse and field trials revealed that qNLB1.06Tx303 reduces the efficiency of fungal penetration, while qNLB1.02B73 enhances the accumulation of callose and phenolics surrounding infection sites, reduces hyphal growth into the vascular bundle and impairs the subsequent necrotrophic colonization in the leaves. The QTL were equally effective in both juvenile and adult plants; qNLB1.06Tx303 showed greater effectiveness in the field than in the greenhouse. In addition to NLB resistance, qNLB1.02B73 was associated with resistance to Stewart’s wilt and common rust, while qNLB1.06Tx303 conferred resistance to Stewart’s wilt. The non-specific resistance may be attributed to pleiotropy or linkage.