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Cogni, R.

Publications and source records attributed to Cogni, R..

6 recordsLinked to original sources

Gene flow weakens genomic clines while selection maintains adaptive loci: two decades of evolution in Drosophila melanogaster natural populations

Spatial genetic clines suggest local adaptation, but whether they persist or erode over evolutionary time remains largely unknown. Here, we use a unique genomic time series collected over several decades to quantify how gene flow and selection jointly shape spatial genomic structure. We analyzed pooled whole-genome sequencing from 16 natural populations of Drosophila melanogaster sampled along the North American east coast between 1997 and 2023, spanning hundreds of generations. We find pronounced homogenization of populations over time, accompanied by a genome-wide loss of clinal variants. Polymorphisms that remained clinal were less steep on chromosome 3R, reflecting declines in the frequency and clinality of major chromosomal inversions. Genomic context modulates this process: clinal SNPs are preferentially lost in regions of high recombination, whereas remaining clines are increasingly concentrated in coding and splice-associated sites. Despite widespread erosion of spatial structure, we detect signatures of selection shared across space at detoxification loci, including cytochrome P450 genes linked to insecticide resistance. Together, our results show widespread homogenization of neutral spatial variation consistent with gene flow, while spatially varying selection has preserved a subset of functionally important loci.

evolutionary biology↗

Virus infection significantly decreases insect fitness: a meta-analysis

Organisms are constantly at risk of being infected by pathogens such as viruses. Adaptations against viral infection include immune defenses encoded within the host genome and associations with defensive symbionts such as Wolbachia. Wolbachia is widely spread among insects, and its success in nature may be due to its antiviral effects, which can benefit hosts if viruses significantly reduce host fitness. Here, we conducted a meta-analysis to assess the degree to which viral infection affects the fitness of insect hosts, and which factors may influence the impact of viral infection on hosts such as if the insect host is a vector or not of viruses that cause diseases in humans and plants, and if the insect is a new or a natural host of a specific virus. We gathered 1,040 effect sizes from 150 studies. Our results show that viruses significantly reduce host fitness, especially their survival. The decrease in host fitness is higher in non-vector than in vector insects, and we found no difference in fitness decrease caused by viral infection between new and natural hosts. Moreover, we found that fitness effects caused by viruses vary between host order and fitness components. In conclusion, our results show that viruses exert severe harmful effects on hosts by decreasing their fitness. In this context, harboring symbionts that confer antiviral protection, such as Wolbachia, can be highly advantageous for hosts, enhancing their fitness. Conversely, Wolbachia can benefit from the presence of viruses, facilitating its spread in insect populations by offering antiviral protection.

ecology↗

Defensive symbionts provide high protection against natural enemies at low cost to hosts: a meta-analysis

Defensive endosymbionts (i.e., endosymbionts that protect hosts against natural enemies) are widespread in terrestrial arthropods, especially insects. Protection against natural enemies may contribute to their successful spread in nature. However, the outcome of host-symbiont interactions (mutualism or parasitism) depend on the balance between the costs and benefits of the interaction and on the ecological conditions experienced by the host, such as the presence or absence of natural enemies. Here, we conducted a meta-analysis to quantitatively assess the costs and benefits of symbiont-mediated protection in terrestrial arthropods. We gathered approximately 3,425 effect sizes from 246 studies. Our results show that in the presence of natural enemies (i.e., hosts infected with pathogens or parasites), symbionts provide protection, positively affecting the fitness of hosts. In the absence of natural enemies, symbionts caused little reduction in host fitness. Overall, symbiont-mediated protection was 7.1 times stronger than the cost observed in the absence of natural enemies, indicating strong protection and little evidence of substantial fitness costs to hosts. Natural enemies attacking symbiont-infected hosts had substantial reduction in their fitness. Moreover, the level of protection and cost for both hosts and natural enemies varies between the fitness components, host families, symbiont species, and natural enemy group. Our results reveal a broad symbiont-mediated protection with little evidence of substantial costs associated, which may help explain the successful spread of symbionts in wild arthropod populations.

ecology↗

The origin and evolution of loqs2: a gene encoding an antiviral dsRNA binding protein in Aedes mosquitoes

Mosquito borne viruses such as dengue, Zika, yellow fever and Chikungunya cause millions of infections every year. These viruses are mostly transmitted by two urban-adapted mosquito species, Aedes aegypti and Aedes albopictus, that appear to be more permissive to arbovirus infections compared to closely related species, although mechanistic understanding remains unknown. Aedes mosquitoes may have evolved specialized antiviral mechanisms that potentially contribute to the low impact of viral infection. Recently, we reported the identification of an Aedes specific double-stranded RNA binding protein (dsRBP), named Loqs2, that is involved in the control of infection by dengue and Zika viruses in Ae. aegypti. Loqs2 interacts with two important co-factors of the RNA interference (RNAi) pathway, Loquacious (Loqs) and R2D2, and seems to be a strong regulator of the antiviral defense. However, the origin and evolution of loqs2 remains unclear. Here, we describe that loqs2 likely originated from two independent duplications of the first dsRNA binding domain (dsRBD) of loquacious that occurred before the radiation of the Aedes Stegomyia subgenus. After its origin, our analyses suggest that loqs2 evolved by relaxed positive selection towards neofunctionalization. In fact, loqs2 is evolving at a faster pace compared to other RNAi components such as loquacious, r2d2 and Dicer-2 in Aedes mosquitoes. Unlike loquacious, transcriptomic analysis showed that loqs2 expression is tightly regulated, almost restricted to reproductive tissues in Ae. aegypti and Ae. albopictus. Transgenic mosquitoes engineered to ubiquitously express loqs2 show massive dysregulation of stress response genes and undergo developmental arrest at larval stages. Overall, our results uncover the possible origin and neofunctionalization of a novel antiviral gene, loqs2, in Aedes mosquitoes that ultimately may contribute to their effectiveness as vectors for arboviruses.

evolutionary biology↗

Natural selection and parallel clinal and seasonal changes in Drosophila melanogaster

Spatial and seasonal variation in the environment are ubiquitous. Environmental heterogeneity can affect natural populations and lead to covariation between environment and allele frequencies. Drosophila melanogaster is known to harbor polymorphisms that change both with latitude and seasons. Identifying the role of selection in driving these changes is not trivial, because non-adaptive processes can cause similar patterns. Given the environment changes in similar ways across seasons and along the latitudinal gradient, one promising approach may be to look for parallelism between clinal and seasonal change. Here, we test whether there is a genome-wide correlation between clinal and seasonal change, and whether the pattern is consistent with selection. Allele frequency estimates were obtained from pooled samples from seven different locations along the east coast of the US, and across seasons within Pennsylvania. We show that there is a genome-wide correlation between clinal and seasonal variation, which cannot be explained by linked selection alone. This pattern is stronger in genomic regions with higher functional content, consistent with natural selection. We derive a way to biologically interpret these correlations and show that around 3.7% of the common, autosomal variants could be under parallel seasonal and spatial selection. Our results highlight the contribution of natural selection in driving fluctuations in allele frequencies in natural fly populations and point to a shared genomic basis to climate adaptation which happens over space and time in D. melanogaster.

evolutionary biology↗

Complex Coding And Regulatory Polymorphisms In A Restriction Factor Determine The Susceptibility Of Drosophila To Viral Infection

It is common to find that major-effect genes are an important cause of variation in susceptibility to infection. Here we have characterised natural variation in a gene called pastrel that explains over half of the genetic variance in susceptibility to the virus DCV in populations of Drosophila melanogaster. We found extensive allelic heterogeneity, with a sample of seven alleles of pastrel from around the world conferring four phenotypically distinct levels of resistance. By modifying candidate SNPs in transgenic flies, we show that the largest effect is caused by an amino acid polymorphism that arose when an ancestral threonine was mutated to alanine, greatly increasing resistance to DCV. Overexpression of the ancestral susceptible allele provides strong protection against DCV, indicating that this mutation acted to improve an existing restriction factor. The pastrel locus also contains complex structural variation and cis-regulatory polymorphisms altering gene expression. We find that higher expression of pastrel is associated with increased survival after DCV infection. To understand why this variation is maintained in populations, we investigated genetic variation surrounding the amino acid variant that is causing flies to be resistant. We found no evidence of natural selection causing either recent changes in allele frequency or geographical variation in frequency, suggesting that this is an old polymorphism that has been maintained at a stable frequency. Overall, our data demonstrate how complex genetic variation at a single locus can control susceptibility to a virulent natural pathogen.

evolutionary biology↗