GABA primes defense responses against Botrytis cinerea in tomato fruit by modulating ethylene and JA signaling pathways

Abstract

This research set out to investigate the potential action mechanism of γ-aminobutyric acid (GABA) in the control of Botrytis cinerea (B. cinerea) in tomato fruit. The findings confirmed that 10 mM GABA treatment effectively lowered the disease incidence and lesion diameter of tomato fruit caused by B. cinerea. Meanwhile, GABA treatment maintained lower electrical conductivity, color change index and lycopene content. GABA alone had little effect on most disease resistance indexes, but it triggered faster and stronger defense responses after B. cinerea infection. These responses included increases in total phenolics and flavonoids accumulation as well as the activities of chitinase (CHI), β-1,3-glucanase (GLU), phenylalanine ammonia lyase (PAL), polyphenol oxidase (PPO), and up-regulated expression of the pathogenesis-related genes (SlPR1, SlPR2a, SlPR2b, SlPR3a, SlPR3b and SlPR-STH2). Furthermore, GABA inhibited the expression of key synthesis genes of ethylene (SlACS2, SlACS4 and SlACO1) and the accumulation of a key metabolic intermediate 1-Aminocyclo-propane-l-carboxylic acid (ACC) in non-infected fruit, leading to a slight reduction in ethylene production. However, it also reduced the ethylene burst carried on by B. cinerea infection at the early storage and restored the ethylene peak at the end of storage. Furthermore, GABA up-regulated the expression level of SlERF6 directly but induced the up-regulation of SlERF2, SlERF.A4, SlERF.B12, SlERF.C6 and SlERF.H9 in a primed manner. In addition, GABA pretreatment markedly enhanced jasmonic acid (JA) content by activating the transcription of JA biosynthetic genes (SlLoxD, SlAOC and SlOPR3), up-regulated the downstream receptor gene SlCOI1 and down-regulated the suppressor gene SlJAZ2. These results demonstrated that tomato fruit treated with GABA can efficiently enhance resistance against B. cinerea through defense priming, and ethylene and JA signaling pathways are involved in this process.