ArticleScientific reports2016
Chlamydia trachomatis growth and development requires the activity of host Long-chain Acyl-CoA Synthetases (ACSLs).
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Inc/GFP chimera protein-based interactomics reveals host cellular interactions of Cps0558, a novel Chlamydia psittaci inclusion protein.Pathogens and disease · 2025Article
- Legionella pneumophila usurps host cell lipids for vacuole expansion and bacterial growth.PLoS pathogens · 2024Article
- Article
- Insights Into the Biogenesis and Emerging Functions of Lipid Droplets From Unbiased Molecular Profiling Approaches.Frontiers in cell and developmental biology · 2022Review
- The Chlamydia trachomatis inclusion membrane protein CT006 associates with lipid droplets in eukaryotic cells.PloS one · 2022Article
- Article
- Lipid droplets and the host-pathogen dynamic: FATal attraction?The Journal of cell biology · 2021Review
- Host membrane lipids are trafficked to membranes of intravacuolar bacteriumProceedings of the National Academy of Sciences of the United States of America · 2020Article
- The multiple functions of the numerousMicrobial cell (Graz, Austria) · 2019Review
- Targeting Long Chain Acyl-CoA Synthetases for Cancer Therapy.International journal of molecular sciences · 2019Review
- Article
- Lipid Droplets: A Significant but Understudied Contributor of Host⁻Bacterial Interactions.Cells · 2019Review
- Proximity-dependent proteomics of the Chlamydia trachomatis inclusion membrane reveals functional interactions with endoplasmic reticulum exit sites.PLoS pathogens · 2019Article
- Article
- Make It a Sweet Home: Responses ofMicrobiology spectrum · 2019Review
- Chlamydia trachomatis regulates growth and development in response to host cell fatty acid availability in the absence of lipid droplets.Cellular microbiology · 2018Article
- Therapeutic Targets in Chlamydial Fatty Acid and Phospholipid Synthesis.Frontiers in microbiology · 2018Review
- Phosphatidylserine decarboxylase CT699, lysophospholipid acyltransferase CT775, and acyl-ACP synthase CT776 provide membrane lipid diversity to Chlamydia trachomatis.Scientific reports · 2017Article
- Exogenous fatty acid metabolism in bacteria.Biochimie · 2017Review
- Manipulation of Host Cholesterol by Obligate Intracellular Bacteria.Frontiers in cellular and infection microbiology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The obligate-intracellular pathogen Chlamydia trachomatis (Ct) has undergone considerable genome reduction with consequent dependence on host biosynthetic pathways, metabolites and enzymes. Long-chain acyl-CoA synthetases (ACSLs) are key host-cell enzymes that convert fatty acids (FA) into acyl-CoA for use in metabolic pathways. Here, we show that the complete host ACSL family [ACSL1 and ACSL3-6] translocates into the Ct membrane-bound vacuole, termed inclusion, and remains associated with membranes of metabolically active forms of Ct throughout development. We discovered that three different pharmacologic inhibitors of ACSL activity independently impede Ct growth in a dose-dependent fashion. Using an FA competition assay, host ACSLs were found to activate Ct branched-chain FAs, suggesting that one function of the ACSLs is to activate Ct FAs and host FAs (recruited from the cytoplasm) within the inclusion. Because the ACSL inhibitors can deplete lipid droplets (LD), we used a cell line where LD synthesis was switched off to evaluate whether LD deficiency affects Ct growth. In these cells, we found no effect on growth or on translocation of ACSLs into the inclusion. Our findings support an essential role for ACSL activation of host-cell and bacterial FAs within the inclusion to promote Ct growth and development, independent of LDs.
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Registered trials
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