RESUMEN
Despite a century of genetic analysis, the evolutionary processes that have generated the patterns of exceptional genetic and phenotypic variation in the model organism Drosophila melanogaster remains poorly understood. In particular, how genetic variation is partitioned within its putative ancestral range in Southern Africa remains unresolved. Here, we study patterns of population genetic structure, admixture, and the spatial structuring of candidate incompatibility alleles across a global sample, including 223 new accessions, predominantly from remote regions in Southern Africa. We identify nine major ancestries, six that primarily occur in Africa and one that has not been previously described. We find evidence for both contemporary and historical admixture between ancestries, with admixture rates varying both within and between continents. For example, while previous work has highlighted an admixture zone between broadly defined African and European ancestries in the Caribbean and southeastern USA, we identify West African ancestry as the most likely African contributor. Moreover, loci showing the strongest signal of introgression between West Africa and the Caribbean/southeastern USA include several genes relating to neurological development and male courtship behavior, in line with previous work showing shared mating behaviors between these regions. Finally, while we hypothesized that potential incompatibility loci may contribute to population genetic structure across the range of D. melanogaster; these loci are, on average, not highly differentiated between ancestries. This work contributes to our understanding of the evolutionary history of a key model system, and provides insight into the partitioning of diversity across its range.
Asunto(s)
Evolución Biológica , Drosophila melanogaster , Animales , Drosophila melanogaster/genética , Alelos , África , Indias Occidentales , Genética de Población , Variación GenéticaRESUMEN
During biological invasions, invasive populations can suffer losses of genetic diversity that are predicted to negatively impact their fitness/performance. Despite examples of invasive populations harboring lower diversity than conspecific populations in their native range, few studies have linked this lower diversity to a decrease in fitness. Using genome sequences, we show that invasive populations of the African fig fly, Zaprionus indianus, have less genetic diversity than conspecific populations in their native range and that diversity is proportionally lower in regions of the genome experiencing low recombination rates. This result suggests that selection may have played a role in lowering diversity in the invasive populations. We next use interspecific comparisons to show that genetic diversity remains relatively high in invasive populations of Z. indianus when compared with other closely related species. By comparing genetic diversity in orthologous gene regions, we also show that the genome-wide landscape of genetic diversity differs between invasive and native populations of Z. indianus indicating that invasion not only affects amounts of genetic diversity but also how that diversity is distributed across the genome. Finally, we use parameter estimates from thermal performance curves for 13 species of Zaprionus to show that Z. indianus has the broadest thermal niche of measured species, and that performance does not differ between invasive and native populations. These results illustrate how aspects of genetic diversity in invasive species can be decoupled from measures of fitness, and that a broad thermal niche may have helped facilitate Z. indianus's range expansion.
Asunto(s)
Drosophilidae/genética , Variación Genética , Especies Introducidas , Animales , Genoma de los Insectos , Temperatura , Secuenciación Completa del GenomaRESUMEN
Paracoccidioidomycosis (PCM) is a life-threatening systemic mycosis widely reported in the Gran Chaco ecosystem. The disease is caused by different species from the genus Paracoccidioides, which are all endemic to South and Central America. Here, we sequenced and analyzed 31 isolates of Paracoccidioides across South America, with particular focus on isolates from Argentina and Paraguay. The de novo sequenced isolates were compared with publicly available genomes. Phylogenetics and population genomics revealed that PCM in Argentina and Paraguay is caused by three distinct Paracoccidioides genotypes, P. brasiliensis (S1a and S1b) and P. restrepiensis (PS3). P. brasiliensis S1a isolates from Argentina are frequently associated with chronic forms of the disease. Our results suggest the existence of extensive molecular polymorphism among Paracoccidioides species, and provide a framework to begin to dissect the connection between genotypic differences in the pathogen and the clinical outcomes of the disease.
Asunto(s)
Variación Genética/genética , Genómica , Paracoccidioides/genética , Paracoccidioidomicosis/genética , Argentina/epidemiología , Ecosistema , Genética de Población , Genoma Fúngico/genética , Genotipo , Humanos , Paracoccidioides/clasificación , Paracoccidioides/patogenicidad , Paracoccidioidomicosis/clasificación , Paracoccidioidomicosis/epidemiología , Paracoccidioidomicosis/microbiología , Paraguay/epidemiología , FilogeniaRESUMEN
Determining mechanisms that underlie reproductive isolation (RI) is key to understanding how species boundaries are maintained in nature. Transposable elements (TEs) are ubiquitous across eukaryotic genomes. However, the role of TEs in modulating the strength of RI between species is poorly understood. Several species of Drosophila have been found to harbor P-elements (PEs), yet only D. simulans is known to be currently polymorphic for their presence in wild populations. PEs can cause RI between PE-containing (P) and PE-lacking (M) lineages of the same species. However, it is unclear whether they also contribute to the magnitude of RI between species. Here, we use the simulans species complex to assess whether differences in PE status between D. simulans and its sister species, which do not harbor PEs, contribute to multiple barriers to gene flow between species. We show that crosses involving a P D. simulans father and an M mother from a sister species exhibit lower F1 female fecundity than crosses involving an M D. simulans father and an M sister-species mother. We also find that another TE, I-element, might play a minor role in determining the frequency of dysgenesis between species. Our results suggest that the presence of PEs in a species can strengthen isolation from its sister species, providing evidence that TEs can play a role in RI.
Asunto(s)
Drosophila simulans , Aislamiento Reproductivo , Animales , Elementos Transponibles de ADN , Drosophila/genética , Drosophila melanogaster/genética , Drosophila simulans/genética , FemeninoRESUMEN
Transposable elements (TEs) are repetitive regions of DNA that are able to self-replicate and reinsert themselves throughout host genomes. Since the discovery of TEs, a prevalent question has been whether increasing TE copy number has an effect on the fitness of their hosts. P-elements (PEs) in Drosophila are a well-studied TE that has strong phenotypic effects. When a female without PEs (M) is crossed to a male with them (P), the resulting females are often sterile, a phenomenon called hybrid dysgenesis (HD). Here, we used short- and long-read sequencing to infer the number of PEs in the genomes of dozens of isofemale lines from two Drosophila species and measured whether the magnitude of HD was correlated with the number of PEs in the paternal genome. Consistent with previous reports, we find evidence for a positive correlation between the paternal PE copy number and the magnitude of HD in progeny from âM × â P crosses for both species. Other crosses are not affected by the number of PE copies. We also find that the correlation between the strength of HD and PE copy number differs between species, which suggests that there are genetic differences that might make some genomes more resilient to the potentially deleterious effects of TEs. Our results suggest that PE copy number interacts with other factors in the genome and the environment to cause HD and that the importance of these interactions is species specific.