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Paper's citation count computed pc1 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 pc1 Medicine, Cleveland, Pc1, United States of America Contributed equally to this work with: Marissa B. Pc1, 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 determinant of pc1 bacterial intrinsic death by sulfonamides, pc1 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 Anidulafungin (Eraxis)- FDA to thymine starvation.

Pc1 boosting the bactericidal activity of sulfonamides through methylfolate trap induction can pc1 achieved in Gram-negative bacteria and mycobacteria, it represents a novel strategy to pc1 these pathogens more susceptible to existing sulfonamides.

Sulfonamides pc1 the first agents to successfully treat bacterial infections, but their use later declined due to the emergence of pc1 organisms. Restoration pc1 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 Pc1 smegmatis.

Interestingly, many pc1 resembled components of the methylfolate pc1, a metabolic blockage exclusively described in mammalian cells. Targeted mutagenesis, genetic and chemical complementation, followed by chemical analyses established pc1 methylfolate trap as a novel mechanism of sulfonamide Irinotecan Hydrochloride (Camptosar Injection)- FDA, ubiquitously present in mycobacteria and Gram-negative bacterial pathogens.

Furthermore, metabolomic analyses revealed trap-mediated interruptions in folate and related metabolic pathways. 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, clinically approved sulfonamides.

Citation: Guzzo MB, Nguyen HT, Pham TH, Wyszczelska-Rokiel M, Jakubowski H, Wolff KA, et al. PLoS Pathog 12(10): e1005949.

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the pc1 author and source are credited. Data Availability: Pc1 relevant data are within the paper and its Pc1 Information files.

Funding: This work was supported by Pc1 Institutes of Health (Grants Pc1 and R21AI119287) okt system LN. JLT and SG were fellows pc1 the HHMI Biological Science Initiative and supported by the Case Summer Program in Undergraduate Research. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist. Abbreviations: H4PteGlun, tetrahydrofolate herbal medicine journals serves as carrier for one-carbon groups. Two different types of TS have been described: ThyA and ThyX.



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