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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 F 2:3 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 in uenced by signi cant Genotype × location interaction. Six and 56 F 2:3 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 signi cant 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.Signi cant di-QTL interactions involving QTL (with signi cant and/or non-signi cant effects) located within and between all the ten chromosomes were detected. Five of the seven detected QTL in our study showed signi cant 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.

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