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Campagne, P.

Publications and source records attributed to Campagne, P..

5 recordsLinked to original sources

Parallel evolution of industrial melanism in the peppered moth: one locus, many alleles

The extent to which adaptation to environmental change occurs via single or multiple advantageous mutations remains an open question, which we examined by studying the spread of melanic forms of the peppered moth in Britain and continental Europe, in response to industrial coal pollution. In Britain, the darkest melanic form is due to the insertion of a transposable element (carb-TE) into a genomic region called ivory. Here, we characterize the spread of melanic forms in continental Europe from historical records and uncover the genetic basis of European melanism using genomic analyses of modern and museum specimens. We show that European melanism is also associated with variants at ivory, but with multiple alleles featuring structural variants, including several transposable elements, though not carb-TE. The primary central European melanic allele is a genetically dominant 805 base pair deletion (sollichau). Interestingly, melanic individuals with either sollichau (deletion) or carb-TE (insertion) alleles show elevated expression of ivory and its effector micro-RNA (mir-193) compared to non-melanic (typica) individuals, suggesting that contrasting structural variants in ivory have similar regulatory effects. A functional role for sollichau was corroborated, serendipitously, by its presence in a typica individual which also contains a linked deletion of mir-193, which is predicted to cancel the melanizing effect of the sollichau deletion. Our results support the idea that there can be many genetic origins of the same adaptive trait within a species, particularly one with a large effective population size and heterogeneous natural habitat, and when many mutations can give rise to the same phenotype.

evolutionary biology↗

A SHERLOCK toolbox for the eco-epidemiological surveillance of animal African trypanosomosis reveals a similar parasite diversity in domestic pigs in two ancient sleeping sickness foci in Western Africa.

Animal African trypanosomosis (AAT), caused by protist parasites of the genus Trypanosoma, puts upward of a million head of livestock at risk across 37 countries in Africa. The economic impact of AAT and the presence of human-infectious trypanosomes in animals place a clear importance on improving diagnostics for animal trypanosomes to map the distribution of the veterinary parasites and identify reservoirs of human-infectious trypanosomes. We have adapted the CRISPR-based detection toolkit SHERLOCK (Specific High-sensitivity Enzymatic Reporter unLOCKing) for trypanosomatid parasites responsible for AAT (SHERLOCK4AAT) including Pan- trypanosomatid, Trypanozoon, T. vivax, T. congolense, T. theileri, T. simiae and T. suis assays. To test the applicability of this technique in the field, we analysed dried blood spots collected from 200 farm and 224 free-ranging pigs in endemic and historical human African trypanosomiasis foci in Guinea and Cote dIvoire, respectively. The results revealed that SHERLOCK4AAT can detect and discriminate between trypanosome species involved in multiple infections with a high sensitivity. 62.7 % [58.1, 67.3] of pigs were found infected with at least one trypanosome species. T. brucei gambiense, a human-infectious trypanosome, was found in one animal at both sites, highlighting the risk that these animals may act as persistent reservoirs. These data suggest that, due to their proximity to humans and their attractiveness to tsetse flies, pigs could act as sentinels to monitor T. b. gambiense circulation using the SHERLOCK4AAT toolbox.

microbiology↗

Global evolutionary patterns of Yersinia pestis and its spread into Africa

The zoonotic pathogen Yersinia pestis, the etiologic agent of plague, has caused three major pandemics and diversified in different lineages currently established in endemic areas worldwide1-3. However, some regions like continental Africa have been poorly covered within the global diversity and epidemiological history of this pathogen2,4-6. Here, we report the whole-genome sequences of 1,124 Y. pestis isolates collected from endemic areas worldwide over 116 years, nearly doubling the available genomic data for the species. By integrating population genomics and historical research, we retrace the introduction of multiple Y. pestis lineages into continental Africa, revealing the diversity of the 1.ANT lineage, its historical emergence and its spread to and within Africa since the late 17th century. We identify key mechanisms of genome evolution, including signatures of adaptive evolution present in virulence and biofilm-related genes such as RovA, a master virulence regulator, which likely play a role in the pathogens adaptation and endemic persistence. Additionally, our findings reveal an increased trajectory of genome degradation and expansion of IS elements in different lineages. This trend appears especially pronounced in 1.ANT genomes, promoting the remarkable genomic variation within this lineage. Taken together, our findings shed light on the introduction and evolutionary history of plague in Africa and provide a comprehensive framework for understanding the global diversity and genome evolution of Y. pestis, revealing potential factors contributing to its long-term adaptation in endemic areas.

microbiology↗

Dynamic microfluidic single-cell screening identifies pheno-tuning compounds to potentiate tuberculosis therapy

Drug-recalcitrant infections are a leading global-health concern. Bacterial cells benefit from phenotypic variation, which can suggest effective anti-microbial strategies. However, probing phenotypic variation entails spatiotemporal analysis of individual cells that is technically challenging, and hard to integrate into drug discovery. To address this, we developed a flow-controlled multi-condition microfluidic platform suitable for imaging two-dimensional growth of bacterial cells, compressed inside separate microchambers by a soft hydro-pneumatic membrane. With this platform, we implemented a dynamic single-cell screening for compounds that induce a phenotypic change while decreasing cell-to-cell variation, aiming to undermine the bacterial population, making it more vulnerable to other drugs. We first applied this strategy to mycobacteria, as tuberculosis poses a major public-health threat. Our top hit impairs Mycobacterium tuberculosis via a peculiar mode of action and enhances other anti-tubercular drugs. This work proves that pheno-tuning compounds represent a successful approach to tackle pathogens that are increasingly difficult to treat.

microbiology↗

The spatial heterogeneity of the gut limits bacteriophage predation leading to the coexistence of antagonist populations of bacteria and their viruses

Bacteria and their viruses, bacteriophages (phages), are the most abundant components of the mammalian gut microbiota where these two entities coexist over time. The ecological dynamics underlying the coexistence between these two antagonistic populations in the gut are unknown. We challenged a murine synthetic bacterial community with a set of virulent phages, to study the factors allowing phages-bacteria coexistence in the gut. We found that coexistence was neither dependent on an arms race between bacteria and phages, nor on the ability of phages to extend host range. Instead, our data suggest that some phage-inaccessible sites in the mucosa of the ileum serve as a spatial refuge for bacteria, which from there disseminate in the gut lumen. Luminal phages amplify by infecting luminal bacteria maintaining phage throughout the gut. We conclude that the heterogeneous distribution of microbes in the gut contributes to the long-term coexistence of phages with phage-susceptible bacteria. This observation could explain the persistence in the human gut of intestinal phages, such as the crAssphage, as well as the low efficiency of oral phage therapy against enteric pathogens in animal models and clinical trials.

microbiology↗