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Polyketide synthase-derived sphingolipids determine microbiota-mediated protection against pathogens in C. elegans

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Drechsler,  Moritz
Natural Product Function and Engineering, Department of Natural Products in Organismic Interactions, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Angelidou,  Georgia
Core Facility Metabolomics and small Molecules Mass Spectrometry, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Paczia,  Nicole       
Core Facility Metabolomics and small Molecules Mass Spectrometry, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Shi,  Yi-Ming
Department of Natural Products in Organismic Interactions, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Bode,  Helge B.       
Natural Product Function and Engineering, Department of Natural Products in Organismic Interactions, Max Planck Institute for Terrestrial Microbiology, Max Planck Society;

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Citation

Peters, L., Drechsler, M., Pees, B., Angelidou, G., Salzer, L., Moors, K. A., et al. (2024). Polyketide synthase-derived sphingolipids determine microbiota-mediated protection against pathogens in C. elegans. bioRxiv: the preprint server for biology, doi: 10.1101/2024.02.06.579051.


Cite as: https://hdl.handle.net/21.11116/0000-000E-5FFA-F
Abstract
Protection against pathogens is a major function of the gut microbiota. Although bacterial natural products have emerged as crucial components of host-microbiota interactions, their exact role in microbiota-mediated protection is largely unexplored. We addressed this knowledge gap with the nematode Caenorhabditis elegans and its microbiota isolate Pseudomonas fluorescens MYb115 that is known to protect against Bacillus thuringiensis (Bt) infection. We find that MYb115-mediated protection depends on sphingolipids that are derived from an iterative type I polyketide synthase (PKS), thereby describing a noncanonical pathway of bacterial sphingolipid production. We provide evidence that MYb115-derived sphingolipids affect C. elegans tolerance to Bt infection by altering host sphingolipid metabolism. This work establishes sphingolipids as structural outputs of bacterial PKS and highlights the role of microbiota-derived sphingolipids in host protection against pathogens.Competing Interest StatementThe authors have declared no competing interest.