Targeted knockout of a host peroxisomal peptidase confers field resistance to maize lethal necrosis

Apr 30, 2026Proceedings of the National Academy of Sciences of the United States of America

Removing a specific cell enzyme in maize helps resist lethal necrosis disease

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Abstract

Targeted knockout of a specific gene in maize conferred resistance to maize lethal necrosis disease in field trials.

Maize lethal necrosis is caused by infections from maize chlorotic mottle virus and a potyvirus, primarily sugarcane mosaic virus.
A major-effect quantitative trait locus for resistance was identified on chromosome 6, derived from the Thai line KS23-6.
Fine mapping and gene editing revealed a peroxisomal enzyme as the cause of susceptibility to the disease.
Knocking out the identified gene in a susceptible maize line resulted in resistance comparable to the resistant line KS23-6.
The knockout specifically inhibited the accumulation of maize chlorotic mottle virus without impacting sugarcane mosaic virus.
Edited maize lines did not show any yield penalty or agronomic defects in disease-free conditions.

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Maize lethal necrosis (MLN) is a severe disease caused by the combined infection of maize chlorotic mottle virus (MCMV) and a potyvirus, most often sugarcane mosaic virus (SCMV). This disease seriously threatens food security across sub-Saharan Africa (SSA). We investigated a major-effect quantitative trait locus for resistance on chromosome 6, named the(), derived from the Thai line KS23-6. Fine mapping and CRISPR-Cas9 editing of the candidate genes within the narrowed 105 kb interval revealed a peroxisomalas the underlying cause of susceptibility. Confocal microscopy confirmed the localization of the MLNS1 protein within peroxisomes. Targeted knockout of thegene in the susceptible elite line CML536 from SSA conferred resistance comparable to KS23-6 in field trials conducted in Naivasha, Kenya. This knockout specifically blocked MCMV accumulation without affecting SCMV. The edited lines showed no yield penalty or agronomic defects under disease-free conditions. Our findings uncover a mechanistic link between a peroxisomal enzyme and viral susceptibility. They also establish a rapid, scalable gene editing strategy for incorporating MLN resistance into elite germplasm, offering a model for combating similar viral diseases in staple crops globally. maize lethal necrosis susceptibility locus 1qMLNS1peptidase Mlns1

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Targeted knockout of a host peroxisomal peptidase confers field resistance to maize lethal necrosis

Abstract

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