Abstract
Late wilt disease (LWD) caused by Harpophora maydis (Samra, Sabet and Hing) is emerging as major production constraint in maize across the world. As a prelude to develop maize hybrids resistance to LWD, genetic basis of resistance was investigated. Two F2:3 mapping populations (derived from CV156670 × 414-33 (P-1) and CV156670 × CV143587 (P-2)) were challenged with LWD at two locations (Kallinayakanahalli and Muppadighatta) during 2017 post-rainy season. Wider range of LWD scores were observed at both locations in both the populations. LWD response was influenced by significant Genotype × location interaction. Six and 56 F2:3 progeny families showed resistance level better than resistant parent. 150 and 199 polymorphic SNP markers were used to genotype P-1 and P-2, respectively. Inclusive composite interval mapping was performed to detect significant QTL, QTL × QTL, QTL × Location interaction effects. Three major and four minor QTL controlling LWD resistance were detected on chromosome-1. Position and effect of the QTL varied with the location. Significant di-QTL interactions involving QTL (with significant and/or non-significant effects) located within and between all the ten chromosomes were detected. Five of the seven detected QTL in our study showed significant QTL × location interaction. Though two major QTL (q-lw-1.5 and q-lw-1.6) with lower Q×L interaction effects could be considered as stable, their phenotypic variance is not large enough to deploy them in MAS. Based on these results, strategies to breed maize for resistance to LWD are discussed.
USE SILICA NANOPARTICLES IN CONTROLLING LATE WILT DISEASE IN MAIZE CAUSED BY HARPOPHORA MAYDIS
