PT  - JOURNAL ARTICLE
AU  - Tatiana Hillman
TI  - Integrating the metabolic processes of &lt;em&gt;Escherichia coli&lt;/em&gt; with virulence by decreasing glucose availability, inhibiting the acetyl-CoA carboxylase gene &lt;em&gt;accA&lt;/em&gt; with asRNA, and through the quantification of the &lt;em&gt;luxs&lt;/em&gt; gene
AID  - 10.1101/747980
DP  - 2019 Jan 01
TA  - bioRxiv
PG  - 747980
4099  - http://biorxiv.org/content/early/2019/10/18/747980.short
4100  - http://biorxiv.org/content/early/2019/10/18/747980.full
AB  - The study aims to demonstrate a possible link between bacterial cell metabolism and virulence by combining the metabolic mechanisms of the gram-negative bacteria, Escherichia coli. Glucose increases the proliferation of intestinal microflora. The bacterial microflora ferment glucose into short-chain fatty acids and long-chain fatty acids. Bacteria synthesize long-chain fatty acids for plasma membrane and biofilm formation. Escherichia coli was cultured in Luria broth, enhanced with a high to a low concentration of glucose to increase the synthesis of acetyl-CoA carboxylase. The 15mM sample yielded 4,210ng/µL of qPCR products measured for the target gene accA. The 7.5mM sample produced a concentration equal to 375 ng/µL, and the control sample measured an accA concentration of 196 ng/µL. The gene accA, one of four subunits for the acetyl-CoA carboxylase enzyme, was suppressed by asRNA, producing a qPCR product of 63 gene copies. Antisense RNA for accA reduced the amount of luxs, a vital gene needed for propagating quorum-sensing signal molecules. The luxs gene, which is responsible for releasing autoinducer-2 for intercellular quorum sensing, was reduced by the gene inhibition of accA with asRNA. The increase in luxs transcription augments biofilm production in support of spreading virulence. An antibiotic resistance test was performed that implanted disk containing tetracycline, carbenicillin, and chloramphenicol unto cultures expressing antisense RNA. Bacterial cells that were transformed with the antisense inducible vector, for inhibiting accA, displayed more antibiotic susceptibility. The implications of the study advocate for designing antibiotics that target bacterial cell metabolic processes to block bacterial antibiotic resistance.