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Paper's citation count computed by Dimensions. PLOS views and downloads. Sum of Facebook, Twitter, Reddit and Wikipedia activity. Contributed equally to this work with: Marissa B. NguyenAffiliation Department of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine, Cleveland, Ohio, United States of America Contributed equally to this work with: Marissa B.

However, the existence or physiological significance of this phenomenon has been unknown in bacteria, which synthesize folate de novo. Here we identify the methylfolate trap as a novel depo injection provera of the bacterial intrinsic death by sulfonamides, antibiotics that block de novo folate synthesis. Genetic mutagenesis, chemical complementation, and metabolomic profiling revealed trap-mediated metabolic imbalances, which induced thymineless death, a phenomenon in which rapidly growing cells succumb to thymine starvation.

Since boosting the bactericidal activity of synthroid no through methylfolate trap induction can be achieved in Gram-negative bacteria and mycobacteria, it represents a novel strategy to render these pathogens more susceptible to existing sulfonamides.

Sulfonamides were the first agents to successfully treat bacterial infections, but their use later declined due to the emergence of resistant organisms. Restoration of these drugs may be achieved through inactivation of molecular mechanisms responsible for resistance.

A chemo-genomic screen first identified 50 chromosomal loci representing the whole-genome antifolate resistance determinants in Mycobacterium smegmatis. Interestingly, many determinants resembled components of the methylfolate trap, a metabolic blockage exclusively described in mammalian cells. Targeted mutagenesis, genetic and chemical complementation, followed by chemical analyses established the methylfolate trap as a novel mechanism of sulfonamide sensitivity, ubiquitously present in mycobacteria and Gram-negative bacterial pathogens.

Furthermore, metabolomic analyses revealed trap-mediated interruptions in folate depo injection provera related metabolic free journal. These metabolic imbalances induced thymineless death, which was reversible with exogenous thymine supplementation. Chemical restriction of vitamin B12, an important molecule required for prevention of the methylfolate trap, sensitized intracellular bacteria to sulfonamides.

Thus, pharmaceutical promotion of the methylfolate trap represents a novel folate antagonistic strategy to render pathogenic bacteria more susceptible to available, depo injection provera approved sulfonamides. Citation: Guzzo MB, Nguyen HT, Pham TH, Wyszczelska-Rokiel M, Jakubowski H, Wolff KA, et al.



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