Kissoyan, Kohar, Dierking, Katja, Drechsler, Moritz, Peters, Lena, Hamerich, Inga, Bode, Helge
[
International Worm Meeting,
2021]
It has become increasingly clear how important gut bacteria are for the protection of the host against invading pathogens. The underlying mechanisms of microbiota-mediated protection, however, are largely unknown. In recent years C. elegans has been established as a model system to study host-microbiota interactions and microbiota-mediated protective effects against pathogens. Our work focuses on two Pseudomonas natural microbiota isolates, Pseudomonas lurida (MYb11) and Pseudomonas fluorescens (MYb115), which have previously been shown to protect C. elegans from infections with Bacillus thuringiensis (MYBt18247) and Pseudomonas aeruginosa (PA14). We are currently characterizing the influence of these microbiota isolates on the lifespan, reproduction, and most importantly, immune defense and aim to understand on how exactly microbiota-mediated protection is induced on both the microbiota and the host side. On the microbiota side, we have identified a biosynthetic gene cluster encoding a type I polyketide synthase (PKS), the resulting natural product induces the protective effect of MYb115 when worms are infected with Bt247. On the host side, we are currently using a reporter gene approach to identify genes and defense pathways involved in the worm response to infection. We will discuss our most recent results at the conference.
[
International Worm Meeting,
2019]
C. elegans is associated in nature with a species-rich, distinct microbiota, which was characterized only recently [1]. Our understanding of C. elegans microbiota function is thus still in its infancy. Here, we identify natural C. elegans microbiota isolates of the Pseudomonas fluorescens subgroup that increase C. elegans resistance to pathogen infection. We show that different Pseudomonas isolates provide paramount protection from infection with the natural C. elegans pathogen Bacillus thuringiensis through distinct mechanisms [2] . The P. lurida isolates MYb11 and MYb12 (members of the P. fluorescens subgroup) protect C. elegans against B. thuringiensis infection by directly inhibiting growth of the pathogen both in vitro and in vivo. Using genomic and biochemical approaches, we demonstrate that MYb11 and MYb12 produce massetolide E, a cyclic lipopeptide biosurfactant of the viscosin group, which is active against pathogenic B. thuringiensis. In contrast to MYb11 and MYb12, P. fluorescens MYb115-mediated protection involves increased resistance without inhibition of pathogen growth and most likely depends on indirect, host-mediated mechanisms. We are currently investigating the molecular basis of P. fluorescens MYb115-mediated protection using a multi-omics approach to identify C. elegans candidate genes involved in microbiota-mediated protection. Moreover, we are further exploring the antagonistic interactions between C. elegans microbiota and pathogens. This work provides new insight into the functional significance of the C. elegans natural microbiota and expands our knowledge of immune-protective mechanisms. 1. Zhang, F., Berg, M., Dierking, K., Felix, M.A., Shapira, M., Samuel, B.S., and Schulenburg, H. (2017). Caenorhabditis elegans as a model for microbiome research. Front. Microbiol. 8:485. 2. Kissoyan, K.A.B., Drechsler, M., Stange, E.-L., Zimmermann, J., Kaleta, C., Bode, H.B., and Dierking, K. (2019). Natural C. elegans Microbiota Protects against Infection via Production of a Cyclic Lipopeptide of the Viscosin Group. Curr. Biol. 29.