|Stuber, Charles - RETIRED|
|Senior, M - SYNGENTA|
Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 29, 2004
Publication Date: August 1, 2004
Citation: Carson, M.L., Stuber, C.W., Senior, M.L. 2004. Identification and mapping of quantitative trait loci conditioning resistance to southern leaf blight of maize caused by Cochliobolus heterostrophus race O. Phytopathology. 94:862-867. Interpretive Summary: Southern leaf blight is an important disease of corn whenever it is grown under warm, humid conditions. Resistant hybrids are the primary means of controlling this disease. Most resistant hybrids rely on resistance that is controlled by many genes, each of which have a small effect. We used modern DNA based markers to determine where these genes or quantitative trait loci (QTL) for resistance are located in the corn genome. Three QTL on three different chromosomes were most important in determining resistance to southern leaf blight. The primary users of this information are corn geneticists and breeders. This information will be useful in using molecular markers to assist breeders in enhancing resistance to southern leaf blight in corn. It will also be useful in future attempts to clone and sequence these resistance genes.
Technical Abstract: A random set of recombinant inbred (RI) lines (F6:7) derived from the cross of the inbred lines Mo17 (resistant) and B73 (susceptible) were evaluated for resistance to southern leaf blight (SLB) caused by Cochliobolus heterostrophus race O. The RI lines were genotyped at a total of 234 SSR, RFLP, or isozyme loci. Field plots of the RI lines were artificially inoculated with an aggressive isolate of C. heterostrophus race O period in each of two growing seasons in North Carolina. Lines were rated for % SLB severity two (1996) or three (1995) times during the grain-filling period. Data were also converted to Areas under the Disease Progress Curve (AUDPC) and analyzed using the Composite Interval Mapping option of PLABQTL program. When means of disease ratings over years were fitted to models, a total of eleven QTL were found to condition resistance to SLB, depending upon which disease ratings were used in the analyses. When the AUDPC data were combined and analyzed over environments, seven QTLs, on chromosomes 1, 2, 3, 4, 7, and 10 were found to come from the resistant parent Mo17. An additional QTL for resistance on chromosome 1 came from the susceptible parent B73. The eight identified QTL accounted for 46% of the phenotypic variation for resistance. QTL X environment interactions were often highly significant, but with one exception, were the result of differences in the magnitude of QTL effects between years and not due to changes in direction of effects. QTLs on the long arm of chromosome1 and chromosomes 2 and 3 had the largest effects, were the most consistently detected and accounted for most of the phenotypic variance. No significant additive X additive epistatic effects were detected. These data support earlier reports of the polygenic inheritance of resistance to southern leaf blight of maize.