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Parthuisot, N.

Publications and source records attributed to Parthuisot, N..

4 recordsLinked to original sources
bioRxiv2026

Wolbachia facilitates the reproduction of a parthenogenetic ladybug

Wolbachia is a bacterial endosymbiont that is primarily transmitted from mother to offspring. To increase their transmission, some strains manipulate their hosts reproduction to favor female offspring, such as by inducing parthenogenesis. Here, we assess whether Wolbachia induces parthenogenesis in recently discovered parthenogenetic populations of the ladybug Nephus voeltzkowi by treating females with an antibiotic. Females from sexual populations, which we show are not infected by Wolbachia, serve as a control. Our results demonstrate that the treatment decreases Wolbachia load, subsequently reducing egg production and development among parthenogenetic females, while having no effect on sexual females. Wolbachia load and reproduction then rebound when the treatment is removed. This suggests that the Wolbachia infection is necessary for successful reproduction in the parthenogenetic females, and it may play a two-part role by facilitating egg laying and late embryo development. The cooccurrence of Wolbachia infection and parthenogenesis in N. voeltzkowi, as well as Wolbachias manipulation of host reproduction makes this a likely candidate of Wolbachia-induced parthenogenesis outside of haplo-diploids. Understanding how Wolbachia can impact diverse insect reproductive systems can shed a light on the extent in which these bacteria can manipulate hosts for their own gain.

evolutionary biology↗
bioRxiv2021

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↗
bioRxiv2020

Step-specific adaptation and trade-off over the course of an infection by GASP-mutation small colony variants

During an infection, parasites face a succession of challenges, each decisive for disease outcome. The diversity of challenges requires a series of parasite adaptations to successfully multiply and transmit from host to host. Thus, the pathogen genotypes which succeed during one step might be counter-selected in later stages of the infection. Using the bacteria Xenorhabdus nematophila and adult Drosophila melanogaster as hosts, we showed that such step-specific adaptations, here linked to GASP mutations in the X. nematophila master gene regulator lrp, exist and can trade-off with each other. We found that nonsense lrp mutations had lowered ability to resist the host immune response, while all classes of mutations in lrp were associated with a decrease in the ability to proliferate during early infection. We demonstrate that reduced proliferation of X. nematophila best explains diminished virulence in this infection model. Finally, decreased proliferation during the first step of infection is accompanied with improved proliferation during late infection, suggesting a trade-off between the adaptations to each step. Step-specific adaptations could play a crucial role in the chronic phase of infections in any diseases that show similar small colony variants (also known as SCV) to X. nematophila. ImportanceWithin-host evolution has been described in many bacterial diseases, and the genetic basis behind the adaptations stimulated a lot of interest. Yet, the studied adaptations are generally focused on antibiotic resistance, rarely on the adaptation to the environment given by the host, and the potential trade-off hindering adaptations to each step of the infection are rarely considered. Those trade-offs are key to understand intra-host evolution, and thus the dynamics of the infection. However, the understanding of these trade-offs supposes a detailed study of host-pathogen interactions at each step of the infection process, with for each step an adapted methodology. Using Drosophila melanogaster as host and the bacteria Xenorhabdus nematophila, we investigated the bacterial adaptations resulting from GASP mutations known to induce small colony variant (SCV) phenotype positively selected within-the-host over the course of an infection, and the trade-off between step-specific adaptations.

evolutionary biology↗