Fig. 7: Schematic illustration of the proposed mechanisms of met-driven metabolic reprogramming against tet(X)-carrying bacteria. | Nature Communications

Fig. 7: Schematic illustration of the proposed mechanisms of met-driven metabolic reprogramming against tet(X)-carrying bacteria.

From: Methionine-driven methylation modification overcomes plasmid-mediated high-level tigecycline resistance

Fig. 7

The left shows the comparative metabolomics network between Tig-R and -S. Colored lines represent the major altered pathways, including several amino acid metabolism pathways, nucleotide metabolism, energy metabolism, and carbohydrate metabolism. The gray sections are derived from Interactive Pathways Explorer 3 (iPath3) annotated pathway backgrounds. The right section depicts the specific mechanism of action of Met-mediated metabolic reprogramming. Briefly, exogenous Met induced the high-level depletion of SAM, which activated 5mC methylation modification at the promoter region of tet(X4), therefore down-regulating the transcription of resistance progress. Meanwhile, exogenous Met promoted the uptake of Tig by upregulating the ΔpH component of bacterial PMF. These actions collectively resensitize tet(X)-carrying multidrug-resistant bacteria to Tig treatment.

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