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

Abstract

Minimizing losses to pests and diseases is essential for producing sufficient food to feed the world's 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. This investigation tested whether induction of resistance by b-aminobutyric acid (BABA) at different developmental stages provides an alternative strategy to protect post-harvest tomato fruit against B. cinerea. Soildrenching plants with BABA once fruit had already formed had no impact on tomato susceptibility to B. cinerea. However, BABA application to seedlings significantly reduced 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 revealed 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 BABA-induced resistance. A final targeted metabolomic analysis detected trace residues of BABA accumulated in the red fruit. Overall, it was demonstrated that BABA induces post-harvest resistance in tomato fruit against B. cinerea with no penalties in yield.

Metabolomics to Exploit the Primed Immune System of Tomato Fruit

“…We investigated whether the treatment of tomato seedlings with BABA could impact fruit development and yield. As described previously [23], no differences were found in fruit size ( Figure 2A), but delayed fruit production ( Figure 2B) and fruit ripening ( Figure 2C,D) were reported. However, it was observed that, at 13 weeks of growth, the proportion of green fruit was statistically significantly higher in BABA-treated plants (40%) compared to control plants (33%) ( Figure 2D), indicating that fruit production did not slowdown in BABA-treated plants after ripening processes had begun ( Figure 2D).…”

“…This implies that the induced resistance state is very specific, which strongly suggests that BABA primes multiple signalling pathways through which such different microbes are resisted in the fruit. Among those metabolic responses, hormonal regulations appear detrimental to BABA-induced immunity [23,24,34]. Accordingly, putative annotation of metabolomic markers indicates that hormone conjugates, including salicylic and jasmonic derivatives, and other defence compounds (i.e., flavonoids), are induced upon infection and BABA treatment ( Table 3).…”

Exogenous β‐aminobutyric acid application attenuates Aspergillus decay, minimizes aflatoxin B1 accumulation, and maintains nutritional quality in fresh‐in‐hull pistachio kernels

“…In recent years, BABA treatment has been used as a promising and safe strategy to enhance fungal decay resistance in strawberry, peach, grape berry, mango, jujube, apple, blueberry fruits, tomato, kiwifruit and pitaya fruits during postharvest life. Enhancing decay resistance in fruits treated with BABA during postharvest life may be ascribed to the maintaining of membrane integrity by reducing membrane‐deteriorating phospholipase D (PLD) and lipoxygenase (LOX) enzyme activity, sufficient intracellular adenosine triphosphate (ATP) providing, triggering reactive oxygen species (ROS) scavenging enzyme activity, fortifying cell wall by promoting phenylpropanoid pathway activity accompanying by impeding cell‐wall deteriorating enzymes activity, eliciting PRs genes expression and enzymes activity by triggering NPR1 genes expression, promoting sucrose, fructose and glucose accumulation useful for providing sufficient intracellular ATP, reducing power nicotinamide adenine dinucleotide phosphate and carbon skeletons, triggering systemic acquired resistance (SAR) representing by higher endogenous salicylic acid (SA) and nitric oxide (NO) accumulation or triggering signaling H 2 O 2 accumulation useful for eliciting PRs genes expression and enzymes activity, and promoting endogenous ABA accumulation useful for callose deposition resulting in cell wall fortifying . In addition to priming function, BABA exhibits direct antifungal activity by disintegrating fungal membrane integrity, represented by higher soluble carbohydrates and protein leakage, resulting in lower spore germination and germ tube elongation, which is beneficial for enhancing decay resistance in fruits and vegetables …”

Chitosan primes plant defence mechanisms againstBotrytis cinerea, including expression of Avr9/Cf-9 rapidly-elicited genes

“…Several elicitors have been described to induce resistance mechanisms in tomato against B. cinerea . For instance, BABA has been demonstrated to provide long-lasting induced resistance against B. cinerea in leaves (Luna et al, 2016) and in fruit (Wilkinson et al, 2018). In addition, the plant defence hormone JA has also been linked to short-term and long-term induced resistance in tomato against B. cinerea (Luna et al, 2016, Worrall et al, 2012).…”