TheC. elegansproteome response to two protectivePseudomonassymbionts

AbstractTheC. elegansnatural microbiota isolatesPseudomonas luridaMYb11 andPseudomonas fluorescensMYb115 protect the host against pathogens through distinct mechanisms. WhileP. luridaproduces an antimicrobial compound and directly inhibits pathogen growth,P. fluorescensMYb115 protects the host without affecting pathogen growth. It is unknown how these two protective microbes affect host biological processes. We used a proteomics approach to elucidate theC. elegansresponse to MYb11 and MYb115. We found that bothPseudomonasisolates increase vitellogenin protein production in young adults, which confirms previous findings on the effect of microbiota onC. elegansreproductive timing. Moreover, theC. elegansresponses to MYb11 and MYb115 exhibit common signatures with the response to other vitamin B12-producing bacteria, emphasizing the importance of vitamin B12inC. elegans-microbemetabolic interactions. We further analyzed signatures in theC. elegansresponse specific to MYb11 or MYb115. We provide evidence for distinct modification in lipid metabolism by both mutualistic microbes. We could identify activation of host pathogen defense responses as MYb11-specific proteome signature and demonstrate that the intermediate filament protein IFB-2 is required for MYb115-mediated protection. These results indicate that MYb11 not only produces an antimicrobial compound, but also activates host antimicrobial defenses, which together might increase resistance to infection. In contrast, MYb115 affects host processes such as lipid metabolism and cytoskeleton dynamics, which might increase host tolerance to infection. Overall, this study provides new insights into the potential mechanisms underlyingC. elegansmicrobiota-mediated protection from pathogen infection.