Northern corn leaf blight, caused by the fungal pathogen Exserohilum turcicum, is a major disease of maize. The first major locus conferring resistance to E. turcicum race 0, Ht1, was identified over 50 years ago, but the underlying gene has remained unknown. We employed a map‐based cloning strategy to identify the Ht1 causal gene, which was found to be a coiled‐coil nucleotide‐binding, leucine‐rich repeat (NLR) gene, which we named PH4GP‐Ht1. Transgenic testing confirmed that introducing the native PH4GP‐Ht1 sequence to a susceptible maize variety resulted in resistance to E. turcicum race 0. A survey of the maize nested association mapping genomes revealed that susceptible Ht1 alleles had very low to no expression of the gene. Overexpression of the susceptible B73 allele, however, did not result in resistant plants, indicating that sequence variations may underlie the difference between resistant and susceptible phenotypes. Modelling of the PH4GP‐Ht1 protein indicated that it has structural homology to the Arabidopsis NLR resistance gene ZAR1, and probably forms a similar homopentamer structure following activation. RNA sequencing data from an infection time course revealed that 1 week after inoculation there was a threefold reduction in fungal biomass in the PH4GP‐Ht1 transgenic plants compared to wild‐type plants. Furthermore, PH4GP‐Ht1 transgenics had significantly more inoculation‐responsive differentially expressed genes than wild‐type plants, with enrichment seen in genes associated with both defence and photosynthesis. These results demonstrate that the NLR PH4GP‐Ht1 is the causal gene underlying Ht1, which represents a different mode of action compared to the previously reported wall‐associated kinase northern corn leaf blight resistance gene Htn1/Ht2/Ht3.
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