Lymphocytic choriomeningitis virus (LCMV) is an Old World mammarenavirus found worldwide because of its association with the house mouse. When LCMV spills over to immunocompetent humans, the virus can cause aseptic meningitis; in immunocompromised persons, systemic infection and death can occur. Central Europe is a strategic location for the study of LCMV evolutionary history and host specificity because of the presence of a hybrid zone (genetic barrier) between 2 house mouse subspecies,
Mus musculus musculus
and
M. musculus domesticus
. We report LCMV prevalence in natural mouse populations from a Czech Republic–Germany transect and genomic characterization of 2 new LCMV variants from the Czech Republic. We demonstrate that the main division in the LCMV phylogenetic tree corresponds to mouse host subspecies and, when the virus is found in human hosts, the mouse subspecies found at the spillover location. Therefore, LCMV strains infecting humans can be predicted by the genetic structure of house mice.
A remarkable gene copy number (CN) arms race system has recently been described in laboratory mice, where Slx;Slxl1 and Sly genes compete over transmission by altering fertilisation success of X and Y chromosome-bearing sperm, respectively. Here, we focus on this system in nature, where natural selection can counter CN/gene product escalation. Our model is house mouse subspecies hybridising in Europe. In some regions, Y chromosomes of the Eastern subspecies have introgressed onto Western genomic backgrounds, accompanied by sex ratio distortion in favour of males, consistent with the inbred-lines suggested mechanism: overabundance of SLY protein expressed by invading Y chromosomes. We take Slx as representative of the X side of this arms race and measure Slx|Sly CN and expression across an ‘Invasion’ transect where Ys introgress and a ‘Control’ transect with negligible introgression. Since we found similar Slx|Sly ratios in both transects, SLY overabundance is unlikely to explain the introgression. However, Slx CN is relatively low in the introgression area, suggesting Slx is less able to combat Sly effects here. Further, deterministic changes in Slx;Sly expression proportions versus CN proportions suggest standing variation for trans regulation of Slx|Sly is being co-opted in nature where their arms race reduces population fitness.
The gastrointestinal microbiota (GM) is considered an important component of the vertebrate holobiont. GM–host interactions influence the fitness of holobionts and are, therefore, an integral part of evolution. The house mouse is a prominent model for GM–host interactions, and evidence suggests a role for GM in mouse speciation. However, previous studies based on short 16S rRNA GM profiles of wild house mouse subspecies failed to detect GM divergence, which is a prerequisite for the inclusion of GM in Dobzhansky–Muller incompatibilities. Here, we used standard 16S rRNA GM profiling in two mouse subspecies, Mus musculus musculus and M. m. domesticus, including the intestinal mucosa and content of three gut sections (ileum, caecum, and colon). We reduced environmental variability by sampling GM in the offspring of wild mice bred under seminatural conditions. Although the breeding conditions allowed a contact between the subspecies, we found a clear differentiation of GM between them, in all three gut sections. Differentiation was mainly driven by several Helicobacters and two H. ganmani variants showed a signal of codivergence with their hosts. Helicobacters represent promising candidates for studying GM–host coadaptations and the fitness effects of their interactions.
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