Comparative transcriptomic and proteomic analysis of the antibacterial activity of emodin on Aeromonas hydrophila

Aeromonas hydrophila is one of the main pathogens in aquaculture. Our previous studies have shown that emodin could inhibit the proliferation of A. hydrophila, however, the underlying mechanism is undetermined. Here we clarified the inhibition mechanism of emodin on A. hydrophila (2.5 mg/ml for 6 hours) with joint-analysis of quantitative transcriptome (RNA-seq) and quantitative proteomics (iTRAQ). A total of 99 differentially expressed genes (DEGs) and their corresponding encoding differentially expressed proteins (DEPs) were identified. Bioinformatic analysis of these DEPs shown that emodin induced oxidative damage and inhibited the expression of key proteins in ribosome, amino acid and fatty acid synthesis pathway of A. hydrophila. Among them, atpE, metK and secB have been identified as the main binding targets of emodin against A. hydrophila. It is noteworthy that three potential targets of emodin binding, atpE, metK and secB, have been identified. Further molecular docking simulations shown that metK exhibited the strongest binding capacity in this process. These findings provide new insights into the molecular mechanism of emodin on antimicrobial activity of A. hydrophila.