Same Invasion, Different Routes: Helminth Assemblages May Favor the Invasion Success of the House Mouse in Senegal

Previous field-based studies have evidenced patterns in gastrointestinal helminth (GIH) assemblages of rodent communities that are consistent with “enemy release” and “spill-back” hypotheses, suggesting a role of parasites in the ongoing invasion success of the exotic house mouse (Mus musculus domesticus) in Senegal (West Africa). However, these findings came from a single invasion route, thus preventing to ascertain that they did not result from stochastic and/or selective processes that could differ across invasion pathways. In the present study, we investigated the distribution of rodent communities and their GIH assemblages in three distinct zones of Northern Senegal, which corresponded to independent house mouse invasion fronts. Our findings first showed an unexpectedly rapid spread of the house mouse, which reached even remote areas where native species would have been expected to dominate the rodent communities. They also strengthened previous insights suggesting a role of helminths in the invasion success of the house mouse, such as: (i) low infestation rates of invading mice by the exotic nematode Aspiculuris tetraptera at invasion fronts—except in a single zone where the establishment of the house mouse could be older than initially thought, which was consistent with the “enemy release” hypothesis; and (ii) higher infection rates by the local cestode Mathevotaenia symmetrica in native rodents with long co-existence history with invasive mice, bringing support to the “spill-back” hypothesis. Therefore, “enemy release” and “spill-back” mechanisms should be seriously considered when explaining the invasion success of the house mouse—provided further experimental works demonstrate that involved GIHs affect rodent fitness or exert selective pressures. Next steps should also include evolutionary, immunological, and behavioral perspectives to fully capture the complexity, causes and consequences of GIH variations along these invasion routes.

Neurological diseases caused by coronavirus infection of the respiratory airways

Infections of the central nervous system (CNS) infections are critical problems for public health. They are caused by several different organisms, including the respiratory coronaviruses (CoVs). CoVs usually infect the upper respiratory tract causing the common cold. However, in infants, and in elderly and immunocompromised persons, they can also affect the lower respiratory tract causing pneumonia and various syndromes of respiratory distress. CoVs also have neuroinvasive capabilities because they can spread from the respiratory tract to the CNS. Once infection begins in the CNS cells, it can cause various CNS problems such as status epilepticus, encephalitis, and long‐term neurological disease. This neuroinvasive properties of CoVs may damage the CNS as a result of misdirected host immune response, which could be associated with autoimmunity in susceptible individuals (virus‐induced neuro‐immunopathology) or associated with viral replication directly causing damage to the CNS cells (virus‐induced neuropathology). In December 2019, a new disease named COVID‐19 emerged which is caused by CoVs. The significant clinical symptoms of COVID‐19 are related to the respiratory system, but they can also affect the CNS, causing acute cerebrovascular and intracranial infections. We describe the possible invasion routes of coronavirus in this review article, and look for the most recent findings associated with the neurological complications in the recently published literature.

Correction to: The genome sequence of the grape phylloxera provides insights into the evolution, adaptation, and invasion routes of an iconic pest

An amendment to this paper has been published and can be accessed via the original article.

Reconstructing the Invasion Route of the P-Element in Drosophila melanogaster Using Extant Population Samples

The P-element, one of the best understood eukaryotic transposable elements, spread in natural Drosophila melanogaster populations in the last century. It invaded American populations first and later spread to the Old World. Inferring this invasion route was made possible by a unique resource available in D. melanogaster: Many strains sampled from different locations over the course of the last century. Here, we test the hypothesis that the invasion route of the P-element may be reconstructed from extant population samples using internal deletions (IDs) as markers. These IDs arise at a high rate when DNA transposons, such as the P-element, are active. We suggest that inferring invasion routes is possible as: 1) the fraction of IDs increases in successively invaded populations, which also explains the striking differences in the ID content between American and European populations, and 2) successively invaded populations end up with similar sets of IDs. This approach allowed us to reconstruct the invasion route of the P-element with reasonable accuracy. Our approach also sheds light on the unknown timing of the invasion in African populations: We suggest that African populations were invaded after American but before European populations. Simulations of TE invasions in spatially distributed populations confirm that IDs may allow us to infer invasion routes. Our approach might be applicable to other DNA transposons in different host species.

Stomatal immunity against fungal invasion comprises not only chitin-induced stomatal closure but also chitosan-induced guard cell death

Many pathogenic fungi exploit stomata as invasion routes, causing destructive diseases of major cereal crops. Intensive interaction is expected to occur between guard cells and fungi. In the present study, we took advantage of well-conserved molecules derived from the fungal cell wall, chitin oligosaccharide (CTOS), and chitosan oligosaccharide (CSOS) to study how guard cells respond to fungal invasion. InArabidopsis, CTOS induced stomatal closure through a signaling mediated by its receptor CERK1, Ca2+, and a major S-type anion channel, SLAC1. CSOS, which is converted from CTOS by chitin deacetylases from invading fungi, did not induce stomatal closure, suggesting that this conversion is a fungal strategy to evade stomatal closure. At higher concentrations, CSOS but not CTOS induced guard cell death in a manner dependent on Ca2+but not CERK1. These results suggest that stomatal immunity against fungal invasion comprises not only CTOS-induced stomatal closure but also CSOS-induced guard cell death.

The genome sequence of the grape phylloxera provides insights into the evolution, adaptation, and invasion routes of an iconic pest

Background Although native to North America, the invasion of the aphid-like grape phylloxera Daktulosphaira vitifoliae across the globe altered the course of grape cultivation. For the past 150 years, viticulture relied on grafting-resistant North American Vitis species as rootstocks, thereby limiting genetic stocks tolerant to other stressors such as pathogens and climate change. Limited understanding of the insect genetics resulted in successive outbreaks across the globe when rootstocks failed. Here we report the 294-Mb genome of D. vitifoliae as a basic tool to understand host plant manipulation, nutritional endosymbiosis, and enhance global viticulture. Results Using a combination of genome, RNA, and population resequencing, we found grape phylloxera showed high duplication rates since its common ancestor with aphids, but similarity in most metabolic genes, despite lacking obligate nutritional symbioses and feeding from parenchyma. Similarly, no enrichment occurred in development genes in relation to viviparity. However, phylloxera evolved > 2700 unique genes that resemble putative effectors and are active during feeding. Population sequencing revealed the global invasion began from the upper Mississippi River in North America, spread to Europe and from there to the rest of the world. Conclusions The grape phylloxera genome reveals genetic architecture relative to the evolution of nutritional endosymbiosis, viviparity, and herbivory. The extraordinary expansion in effector genes also suggests novel adaptations to plant feeding and how insects induce complex plant phenotypes, for instance galls. Finally, our understanding of the origin of this invasive species and its genome provide genetics resources to alleviate rootstock bottlenecks restricting the advancement of viticulture.

Reconstructing the invasion route of DNA transposons using extant population samples

Reconstructing invasion routes of transposable elements (TEs), so far, required capturing an ongoing invasion with population samples from different geographic regions and time points. Here, we propose a more accessible approach. Abundantly occurring internal deletions of DNA transposons allow to trace the direction as well as the path of an invasion, even hundreds of generations after the spread of a TE. We validated this hypothesis with computer simulations and by accurately reproducing the route of the P-element invasion in Drosophila melanogaster. Finally, we used our method to shed light on the controversial hobo invasion in D. melanogaster. Our approach solely requires sequenced samples from extant populations and sequences of TEs of interest. Hence, DNA transposons in a wide range of model and non-model organisms may be analyzed. Our approach will further our understanding of TE dynamics, migration patterns, and the ecology of species.