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Adult plant resistance (APR) is an enigmatic phenomenon in which resistance genes are ineffective in protecting seedlings from disease but confer robust resistance at maturity. Maize has multiple cases in which genes confer APR to northern leaf spot, a lethal disease caused by  Cochliobolus carbonum  race 1 (CCR1). The first identified case of APR in maize is encoded by a hypomorphic allele,  Hm1   A  , at the  hm1  locus. In contrast, wild-type alleles of  hm1  provide complete protection at all developmental stages and in every part of the maize plant.  Hm1  encodes an NADPH-dependent reductase, which inactivates HC-toxin, a key virulence effector of CCR1. Cloning and characterization of  Hm1   A   ruled out differential transcription or translation for its APR phenotype and identified an amino acid substitution that reduced HC-toxin reductase (HCTR) activity. The possibility of a causal relationship between the weak nature of  Hm1   A   and its APR phenotype was confirmed by the generation of two new APR alleles of  Hm1  by mutagenesis. The HCTRs encoded by these new APR alleles had undergone relatively conservative missense changes that partially reduced their enzymatic activity similar to HM1 A . No difference in accumulation of HCTR was observed between adult and juvenile plants, suggesting that the susceptibility of seedlings derives from a greater need for HCTR activity, not reduced accumulation of the gene product. Conditions and treatments that altered the photosynthetic output of the host had a dramatic effect on resistance imparted by the APR alleles, demonstrating a link between the energetic or metabolic status of the host and disease resistance affected by HC-toxin catabolism by the APR alleles of HCTR.

Adult plant resistance in maize to northern leaf spot is a feature of partial loss-of-function alleles of Hm1