QTL mapping of resistance to sorghum downy mildew in maize
Sorghum downy mildew (SDM) of maize is caused by the oomycete Peronosclerospora sorghi (Weston and Uppal) C. G. Shaw. The disease can cause devastating yield losses in maize (Zea mays L.). Quantitative trait loci (QTLs) mediating resistance to SDM were mapped using both restriction fragment length polymorphisms (RFLPs), and simple sequence repeats (SSRs) in 220 F2 individual maize progeny derived from a cross between two extremes; highly susceptible inbred parent SC-TEP5-19-1-3-1-4-1-1 (white) and highly resistant inbred P345C4S2B46-2-2-1-2-B-B-B (yellow). The phenotypic expression was assessed on F2:3 families in a wide range of environments under natural field infection and in a controlled greenhouse screening method. Heritability estimates of disease reaction ranged from 93.3% in Thailand sit 1 to 48% in Thailand sit 2. One hundred and thirty three polymorphic markers were assigned to the ten chromosomes of maize with LOD scores exceeding 4.9 covering about 1265 cM with an average interval length between markers of 9.5 cM. About 90% of the genome was located within a 10 cM distance to the nearest marker. Three putative QTLs were detected in association with resistance to SDM in different environments using composite interval mapping. Despite environmental and symptom differences, one QTL on chromosome 2 bin 9 had a major effect in all trials and explained up to 70% of the phenotypic variation in Thailand where the highest disease pressure was experienced. Two other QTLs on chromosome 3 bin 5 and chromosome 9 bin 2 had a minor effect, each explaining no more than 4% of the phenotypic variation. These results revealed one major gene and two minor genes that control sorghum downy mildew resistance. These markers should be very useful in breeding programs in facilitating the introgression of the resistance genes into commercial varieties. Marker-assisted selection for these loci should be useful in incorporating SDM resistance genes in maize across environments, even in the absence of the pathogen.