Long-lasting β-aminobutyric acid-induced resistance protects tomato fruit against Botrytis cinerea

Minimising losses to pests and diseases is essential for producing sufficient food to feed our rapidly growing population. The necrotrophic fungus Botrytis cinerea triggers devastating pre- and post-harvest yield losses in tomato (Solanum lycopersicum). Current control methods are based on the pre-harvest use of fungicides, which are limited by strict legislation. Here, we have tested whether induction of resistance by β-aminobutyric acid (BABA) at different developmental stages, provides an alternative strategy to protect tomato fruit post-harvest against B. cinerea. Soil-drenching plants with BABA once fruit had already formed, had no impact on tomatoes susceptibility to B. cinerea. Whereas BABA application to seedlings was found to significantly reduce the post-harvest infection of fruit. This resistance response was not associated with a yield reduction, however there was a delay in fruit ripening. Untargeted metabolomics unravelled differences between fruit from water and BABA-treated plants, demonstrating that BABA triggered a defence-associated metabolomics profile that was long-lasting. Targeted analysis of defence hormones suggested a role of abscisic acid (ABA) in the resistance phenotype. Post-harvest application of ABA to the fruit of water-treated plants induced susceptibility to B. cinerea. This phenotype was absent from the ABA exposed fruit of BABA-treated plants, suggesting a complex role of ABA in the BABA-induced resistance phenotype. A final targeted metabolomic analysis detected trace residues of BABA accumulated in the red fruit. Overall, we have demonstrated that β-aminobutyric acid induces post-harvest resistance in tomato fruit against B. cinerea with no penalties in yield.