Induction of Direct or Priming Resistance against Botrytis cinerea in Strawberries by β-Aminobutyric Acid and Their Effects on Sucrose Metabolism

The specific forms of disease resistance induced by beta-aminobutyric acid (BABA) and their impacts on sucrose metabolism of postharvest strawberries were determined in the present research. Treatment with 10-500 mmol L-1 BABA inhibited the Botrytis cinerea infection, possibly directly by suppressing the fungus growth and indirectly by triggering disease resistance. Moreover, BABA-induced resistance against B. cinerea infection in strawberries was associated with either one of two mechanisms, depending upon the concentration used: BABA at concentrations higher than 100 mmol L-1 directly induced the defense response, including a H2O2 burst, modulation of the expression of PR genes, including FaPR1, FaChi3, Fa beta glu, and FaPAL, and increased activities of chitinase, beta-1,3-glucanase, and PAL, whereas BABA at 10 mmol L-1 activated a priming response because the BABA-treated fruits exhibited an increased capacity to express molecular defense only when the fruits were inoculated with B. cinerea. Activation of the priming defense appeared almost as effective against B. cinerea as inducing direct defense. However, the primed strawberries maintained higher activities of SS synthesis and SPS and SPP enzymes) and lower level of SS cleavage during the incubation; these activities contributed to higher sucrose, fructose, and glucose contents, sweetness index, and sensory scores compared to fruits exhibiting the direct defense. Thus, it is plausible that the priming defense, which can be activated by BABA at relatively low concentrations, represents an optimal strategy for combining the advantages of enhanced disease protection and soluble sugar accumulation.