Mechanisms of C. elegans microbiota-mediated protection

Microorganisms live in close association with multicellular organisms, with which they form complex networks of interdependent relationships. This microbiota is essential in protecting the host against pathogen infection, commonly referred to as colonization resistance or microbiota-mediated protection. Although microbiota-mediated protection is a well-known phenomenon, the underlying molecular mechanisms remain largely unknown. This thesis aims to comprehensively understand these mechanisms, focusing on the two natural microbiota isolates Pseudomonas lurida MYb11 and Pseudomonas fluorescens MYb115 of the host model organism Caenorhabditis elegant. Using a reductionist approach, I individually exposed the worm to these isolates, revealing diverse effects on life history traits. MYb115 demonstrated neutrality, while MYb11 acted as a pathobiont, shortening lifespan but enhancing fertility. MYb11 increased the abundance of proteins related to the innate immune response, suggesting it primes C. elegans' immune system. MYb115 influenced intestinal cell components, fortifying the epithelial barrier for indirect protection. Importantly, MYb115-mediated protection relied on the non-canonical MYb115 iterative type 1 polyketide synthase biosynthesis gene cluster, producing bacterial sphingolipids. These sphingolipids influenced C. elegans tolerance to Bt247 infection by altering host sphingolipid metabolism. Microbiota-derived sphingolipids emerged as crucial outputs of bacterial polyketide synthase, demonstrating their role in host protection. This thesis enhances our understanding of microbiota-mediated protection, unraveling mechanisms from both host and bacterial perspectives.


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