Sorghum downy mildew caused by Peronosclerospora sorghi is a major disease of maize and resistance is under the control of polygenes which necessitated identification of quantitative-trait loci (QTLs) for initiating marker-assisted introgression of resistant QTLs in elite susceptible inbred lines. In the present study, QTLs for sorghum downy mildew (SDM) resistance in maize were identified based on cosegregation with linked simple sequence repeats in 185 F₂ progeny from a cross between susceptible (CM500-19) and resistant (MAI105) parents. F₃ families were screened in the National Sorghum Downy Mildew Screening Nursery during 2010 and 2011. High heritability was observed for the disease reaction. The final map generated using 87 SSR markers had 10 linkage groups, spanning a length of 1210.3 cM. Although, we used only 87 SSR markers for mapping, the per cent of genome within 20 cM to the nearest marker was 88.5. Three putative QTLs for SDM resistance were located on chromosomes 3 (bin 3.01), 6 (bin 6.01) and 2 (bin 2.02) using composite interval mapping. The locus on chromosome 3 had a major effect and explained up to 12.6% of the phenotypic variation. The other two QTLs on chromosomes 6 and 2 had minor effects with phenotypic variation of 7.1 and 2%. The three QTLs appeared to have additive effects on resistance. The QTLs on chromosomes 3 and 6 were successfully used in the marker-assisted selection programme for introgression of resistance to SDM in eight susceptible maize lines.

The expressed sequence tags (ESTs) of common bean were BLAST aligned with barred medic genome sequence and developed 1196 conserved intron spanning primers (CISPs) to facilitate genetic studies in legumes. Randomly selected 288 CISPs, representing loci on barrel medic genome, were tested on 10 selected members of legume family. On the source taxa, the highest single copy amplification success rates of 61.8% (barrel medic) and 56.2% (common bean) was obtained. The success rate of markers was 54.5% in cowpea followed by 53.5% in pigeonpea and chickpea, signifying cross taxon amplification and their potential use in comparative genomics. However, relatively low percentages of primer set amplified (40–43%) in soybean, urdbean and peanut. Further, these primers were tested on different varieties of chickpea, pigeonpea and cowpea. The PCR products were sequenced and aligned which resulted in detection of 26 SNPs and eight INDeLs in cowpea, seven SNPs and two INDeLs in chickpea and 27 SNPs and 14 INDeLs in pigeonpea. These SNPs were successfully converted in to size variation for gel-based genotyping. The CISP markers developed in this study are expected to aid in map saturation of legumes and in marker-assisted selection for accelerated crop improvement.

Fusarium stalk rot disease (FSR) of maize caused by Fusarium verticillioides (Sacc.) Nirenberg is becoming an importantbiotic production constraint in many of the major maize growing areas causing substantial yield losses. Inbreds are preferred as parents inhybrid development owing to homozygous nature and high heterotic ability. Double haploid (DH) technology has emerged as a significantmilestone. A total of 339 DH lines were generated from two inbred lines, VL1043 (susceptible) and CM212 (resistant), through in vivohaploid induction method. The 339 DH lines along with parents were phenotyped for their response to the FSR at the College ofAgriculture, V. C. Farm, Mandya, India during summer, kharif and rabi seasons of the 2019–2020. Best linear unbiased predictors (BLUPs)were estimated for the FSR disease scores over three seasons. Awide range of BLUP scores of three to nine indicated the presence of highervariation for response of DH lines to FSR disease. The higher estimates of standardized range (1.31) and phenotypic coefficient of variation(19.80) also displayed higher variability. Nine lines were moderately resistant and 188 exhibited moderately susceptible reaction. Thedistribution of DH lines was positively skewed (1.34) and platykurtic (2.31) which suggested complementary epistasis and involvement oflarge number of genes in the disease expression.