ArticleThe Journal of biological chemistry2014
Type II fatty acid synthesis is essential for the replication of Chlamydia trachomatis.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 56 citations in OpenAlex.
- A pilot study of re-purposing drugs to treat koalas with chlamydia.Scientific reports · 2025Article
- A multi-strategy antimicrobial discovery approach reveals new ways to treat Chlamydia.PLoS biology · 2025Article
- Metabolic model guided CRISPRi identifies a central role for phosphoglycerate mutase inmSystems · 2024Article
- HtrA, fatty acids, and membrane protein interplay inJournal of bacteriology · 2024Article
- Lipid-Centric Approaches in Combating Infectious Diseases: Antibacterials, Antifungals and Antivirals with Lipid-Associated Mechanisms of Action.Antibiotics (Basel, Switzerland) · 2023Review
- Article
- Mining Fatty Acid Biosynthesis for New Antimicrobials.Annual review of microbiology · 2022Review
- Genetic susceptibility loci forFrontiers in immunology · 2022Article
- Article
- Molecular causes of an evolutionary shift along the parasitism-mutualism continuum in a bacterial symbiont.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Modulation of Host Lipid Pathways by Pathogenic Intracellular Bacteria.Pathogens (Basel, Switzerland) · 2020Review
- Structural approaches to pathway-specific antimicrobial agents.Translational research : the journal of laboratory and clinical medicine · 2020Review
- The genome of a Bacteroidetes inhabitant of the human gut encodes a structurally distinct enoyl-acyl carrier protein reductase (FabI).The Journal of biological chemistry · 2020Article
- Article
- Biochemical and Structural Insights Concerning Triclosan Resistance in a Novel YXScientific reports · 2019Article
- Biochemical and Structural Basis of Triclosan Resistance in a Novel Enoyl-Acyl Carrier Protein Reductase.Antimicrobial agents and chemotherapy · 2018Article
- Therapeutic Targets in Chlamydial Fatty Acid and Phospholipid Synthesis.Frontiers in microbiology · 2018Review
- Exogenous fatty acid metabolism in bacteria.Biochimie · 2017Review
- N-Acylated Derivatives of Sulfamethoxazole Block Chlamydia Fatty Acid Synthesis and Interact with FabF.Antimicrobial agents and chemotherapy · 2017Article
- Enoyl-Acyl Carrier Protein Reductase I (FabI) Is Essential for the Intracellular Growth of Listeria monocytogenes.Infection and immunity · 2016Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The major phospholipid classes of the obligate intracellular bacterial parasite Chlamydia trachomatis are the same as its eukaryotic host except that they also contain chlamydia-made branched-chain fatty acids in the 2-position. Genomic analysis predicts that C. trachomatis is capable of type II fatty acid synthesis (FASII). AFN-1252 was deployed as a chemical tool to specifically inhibit the enoyl-acyl carrier protein reductase (FabI) of C. trachomatis to determine whether chlamydial FASII is essential for replication within the host. The C. trachomatis FabI (CtFabI) is a homotetramer and exhibited typical FabI kinetics, and its expression complemented an Escherichia coli fabI(Ts) strain. AFN-1252 inhibited CtFabI by binding to the FabI·NADH complex with an IC50 of 0.9 μM at saturating substrate concentration. The x-ray crystal structure of the CtFabI·NADH·AFN-1252 ternary complex revealed the specific interactions between the drug, protein, and cofactor within the substrate binding site. AFN-1252 treatment of C. trachomatis-infected HeLa cells at any point in the infectious cycle caused a decrease in infectious titers that correlated with a decrease in branched-chain fatty acid biosynthesis. AFN-1252 treatment at the time of infection prevented the first cell division of C. trachomatis, although the cell morphology suggested differentiation into a metabolically active reticulate body. These results demonstrate that FASII activity is essential for C. trachomatis proliferation within its eukaryotic host and validate CtFabI as a therapeutic target against C. trachomatis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.