A pathogen-induced translational shift enhances plant disease resistance without obvious fitness costs

Exploring immune mechanisms in plants opens new avenues for engineering disease resistance in crops. Approaches such as the ectopic expression of resistance genes are frequently associated with fitness costs, rendering the resulting germplasm less desirable for agricultural applications. Inducible production of resistance factors is one potential workaround for this problem. In this study, we determined that the 5ʹ untranslated region (5ʹ UTR) of Arabidopsis ( Arabidopsis thaliana ) PI4KIII β1 undergoes a translational shift that alters its translation initiation site upon the activation of immunity. Based on this discovery, we developed a PI4KIII β1 5ʹ UTR cassette to specifically regulate the expression of the hypersensitive induced reaction gene HIR1 , which encodes a cell death-inducing protein. Under normal conditions, ribosomes initiated translation from the first start codon in the PI4KIII β1 5ʹ UTR cassette; however, upon pathogen challenge, the ribosomes bypassed this site and instead initiated translation from a downstream start codon, enabling HIR1 expression. Transgenic Arabidopsis plants harboring the PI4KIII β1 5ʹ UTR cassette driving HIR1 exhibited enhanced disease resistance without detectable changes in key agricultural traits. Therefore, precisely regulating translation initiation through leaky ribosome scanning represents a promising strategy for developing pathogen-resistant crops without obvious fitness costs.