NAC (NAM, ATAF1/2 and CUC2) is a transcription factor which contributes to the response for both biotic and abiotic stresses. In this study, the regulatory effects and potential mechanisms of SNAC4/9 on resistance to Botrytis cinerea (B. cinerea) were investigated by the differences in physiological and biochemical indices as well as transcriptional and metabolic profiles between SNAC4/9 overexpressed (OE-SNAC4/9) and wild-type (WT) tomato fruit inoculated with B. cinerea. The results showed that OE-SNAC4/9 accelerated the infection to tomato fruit by B. cinerea. Specifically, OE-SNAC4/9 mediated the differential expression of genes related to defense signaling such as ROS, phytohormones (SA and JA) and MAPK cascade, and inhibited the activities of PAL, CHI and GLU. Additionally, SNAC4/9 altered the metabolic flux redirection in each branch pathway of phenylpropane metabolism by regulating the expression of 4CL, CHS1/2, FLS and F3H, with overexpression of SNAC4/9 leading to a decrease in the accumulation of rutin, quercetin, naringenin chalcone and naringenin in tomato fruit. In conclusion, SNAC4/9 may inhibit tomato fruit resistance to B. cinerea by modulating signaling, inhibiting PRs (pathogenesis related proteins) synthesis, and altering metabolic flux flow.
Keywords: Botrytis cinerea; Metabolomics; SNAC4/9; Tomato fruit; Transcriptomics.
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