L-Aspartate and L-Glutamine Inhibit Beta-Aminobutyric Acid-Induced Resistance in Tomatoes

Plant diseases caused by pathogens lead to economic and agricultural losses, while plant resistance is defined by robustness and timing of defence response. Exposure to microbial-associated molecular patterns or specific chemical compounds can promote plants into a primed state with more robust defence responses. beta-aminobutyric acid (BABA) is an endogenous stress metabolite that induces resistance, thereby protecting various plants' diverse stresses by induction of non-canonical activity after binding into aspartyl-tRNA synthetase (AspRS). In this study, by integrating BABA-induced changes in selected metabolites and transcript data, we describe the molecular processes involved in BABA-induced resistance (BABA-IR) in tomatoes. BABA significantly restricted the growth of the pathogens P. syringae pv. tomato DC3000 and was related to the accumulation of transcripts for pathogenesis-related proteins and jasmonic acid signalling but not salicylic acid signalling in Arabidopsis. The resistance was considerably reduced by applying amino acids L-Asp and L-Gln when L-Gln prevents general amino acid inhibition in plants. Analysis of amino acid changes suggests that BABA-IR inhibition by L-Asp is due to its rapid metabolisation to L-Gln and not its competition with BABA for the aspartyl-tRNA synthetase (AspRS) binding site. Our results showed differences between the effect of BABA on tomatoes and other model plants. They highlighted the importance of comparative studies between plants of agronomic interest subjected to treatment with BABA.

Automated summary

The study described the molecular processes involved in BABA-induced resistance in tomatoes by analyzing changes in selected metabolites and transcript data induced by BABA, as well as highlighting the impact of BABA on pathogenesis-related proteins and jasmonic acid signaling in Arabidopsis. Additionally, the research found that amino acids L-Asp and L-Gln significantly reduced resistance levels, with the inhibition of BABA-IR due to the rapid metabolization of L-Asp to L-Gln.