Glutamate-pantothenate pathway promotes antibiotic resistance of Edwardsiella tarda.

Although cellular metabolic states have been shown to modulate bacterial susceptibility to antibiotics, the interaction between glutamate (Glu) and chloramphenicol (CAP) resistance remains unclear because of the specificity of antibiotics and bacteria. We found that the level of Glu was upregulated in the CAP-resistant strain of Edwardsiella tarda according to a comparative metabolomics approach based on LC-MS/MS. Furthermore, we verified that exogenous metabolites related to Glu, the tricarboxylic acid (TCA) cycle, and glutathione (GSH) metabolism could promote CAP resistance in survival assays. If GSH metabolism or the TCA cycle is inhibited by L-buthionine sulfoximine or propanedioic acid, the promotion of CAP resistance by Glu in the corresponding pathway disappears. According to metabolomic analysis, exogenous Glu could change pantothenate metabolism, affecting GSH biosynthesis and the TCA cycle. These results showed that the glutamate-pantothenate pathway could promote CAP resistance by being involved in the synthesis of GSH, entering the TCA cycle by direct deamination, or indirectly affecting the metabolism of the two pathways by pantothenate. These results extend our knowledge of the effect of Glu on antibiotic resistance and suggest that the potential effect, which may aggravate antibiotic resistance, should be considered before Glu and GSH administration in the clinic.

Metabolites in the TCA Cycle Promote Resistance to Chloramphenicol of Edwardsiella tarda.

Antibiotic-resistant bacteria are a serious threat to human and animal health. Metabolite-enabled eradication of drug-resistant pathogens is an attractive strategy, and metabolite adjuvants, such as fumarate, are used for restoring the bactericidal ability of antibiotics. However, we show that metabolites in the TCA cycle increase the viability of Edwardsiella tarda against chloramphenicol (CAP), based on the survival assay of differential metabolites identified by LC-MS/MS. Furthermore, NADPH promotes CAP resistance in the CAP-resistant strain, while oxidants restore the bactericidal ability. Finally, we show that the intracellular redox state determines the sensitivity to CAP, and the total antioxidative capacity is decreased significantly in the antibiotic-resistant strain. Considering that the metabolites promote CAP resistance, metabolite adjuvants should be applied very cautiously. Overall, our research expands on the knowledge that the redox state is related to the bactericidal ability of CAP.

The complete mitochondrial genome of two different colour Luciobarbus capito (Cypriniformes, Cyprinidae).

We sequenced and characterized the complete mitochondrial genome from normal colour (grey black) and mutant colour (orangey red) of Luciobarbus capito. Both mitogenomes contained the typical complement of 13 protein-coding genes, 22 transfer RNAs (tRNAs), two ribosomal RNAs (rRNAs), and a non-coding control region. They share the same gene arrangement pattern that was identical with most vertebrates. The entire mitochondrial DNA molecule of grey black L. capito was 16603-bp long, while the complete mtDNA molecule of orangey red L. capito was 16607-bp long.

The complete mitochondrial genome of golden yellow snakehead fish, Channa argus.

We sequenced and characterized the complete mitochondrial genome of golden yellow snakehead fish, Channa argus. The mitogenomes contained the typical complement of 13 protein-coding genes, 22 transfer RNAs (tRNAs), 2 ribosomal RNAs (rRNAs), and a non-coding control region. They share the same gene arrangement pattern that was identical with most vertebrates. The entire mitochondrial DNA molecule of golden yellow snakehead fish was 16,558 bp long. All information reported in this article will be a useful source of sequence information for general molecular and evolutionary studies of the family Channidae.