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FERDY, J.-B.

Publications and source records attributed to FERDY, J.-B..

2 recordsLinked to original sources

Transitive interactions among rhizobia determine their symbiotic fitness

During host-microbe symbioses, the fitness of mutualistic microbes is determined by the interactions that concurrently occur, throughout their life cycle, with their host and other members of the surrounding microbial community. Disentangling how these multiple interactions shape the fitness of microbial symbionts is challenging, but is essential to understand the diversity and functioning of mutualisms. Here we examined the different fitness components of rhizobial symbionts of the legume plant Mimosa pudica across the multiple stages of their symbiotic life cycle. By comparing rhizobial symbiotic fitness in single and pairwise inoculations, we found that inter-bacterial interactions causing significant fitness effects are common, transitive and can have major consequences, sometimes leading to the extinction of a strain. These interactions predominantly occur at the root infection (nodulation) step, but smaller post-infection interaction effects, involving yet uncharacterized mechanisms, were also detected. Furthermore, considering pairwise interactions was sufficient to predict fitness ranks in more complex rhizobial communities consisting of 6 or 8 strains, indicating that higher-order interaction effects do not play a significant role in these communities. Overall, our results provide a quantitative framework to describe the main drivers of rhizobial symbiotic fitness in a simple community context.

microbiology↗

A within-host infection model to explore tolerance andresistance

How are some individuals surviving infections while others die? The answer lies in how infected individuals invest into controlling pathogen proliferation and mitigating damage, two strategies respectively called resistance and disease tolerance. Pathogen within-host dynamics (WHD), influenced by resistance, and its connection to host survival, determined by tolerance, decide the infection outcome. To grasp these intricate effects of resistance and tolerance, we used a deterministic theoretical model where pathogens interact with the immune system of a host. The model describes the positive and negative regulation of the immune response, consider the way damage accumulate during the infection and predicts WHD. When chronic, infections stabilize at a Set-Point Pathogen Load (SPPL). Our model predicts that this situation can be transient, the SPPL being then a predictor of life span which depends on initial condition (e.g. inoculum). When stable, the SPPL is rather diagnostic of non lethal chronic infections. In lethal infections, hosts die at a Pathogen Load Upon Death (PLUD) which is almost independent from the initial conditions. As the SPPL, the PLUD is affected by both resistance and tolerance but we demonstrate that it can be used in conjunction with mortality measurement to distinguish the effect of disease tolerance from that of resistance. We validate empirically this new approach, using Drosophila melanogaster and the pathogen Providencia rettgeri. We found that, as predicted by the model, hosts that were wounded or deficient of key antimicrobial peptides had a higher PLUD, while Catalase mutant hosts, likely to have a default in disease tolerance, had a lower PLUD.

evolutionary biology↗