Recent beak evolution in North American starlings after invasion.

European starlings are one of the most abundant and problematic avian invaders in the world. From their native range across Eurasia and North Africa, they have been introduced to every continent except Antarctica. In 160 years, starlings have expanded into different environments throughout the world, making them a powerful model for understanding rapid evolutionary change and adaptive plasticity. Here, we investigate their spatiotemporal morphological variation in North America and the native range. Our dataset includes 1217 specimens; a combination of historical museum skins and modern birds. Beak length in the native range has remained unchanged during the past 206 years, but we find beak length in North American birds is now 8% longer than birds from the native range. We discuss potential drivers of this pattern including dietary adaptation or climatic pressures. Additionally, body size in North American starlings is smaller than those from the native range, which suggests a role for selection or founder effect. Taken together, our results indicate rapid recent evolutionary change in starling morphology coincident with invasion into novel environments.

Contrasting mitochondrial diversity of European starlings (Sturnus vulgaris) across three invasive continental distributions.

European starlings (Sturnus vulgaris) represent one of the most widespread and problematic avian invasive species in the world. Understanding their unique population history and current population dynamics can contribute to conservation efforts and clarify evolutionary processes over short timescales. European starlings were introduced to Central Park, New York in 1890, and from a founding group of about 100 birds, they have expanded across North America with a current population of approximately 200 million. There were also multiple introductions in Australia in the mid-19th century and at least one introduction in South Africa in the late 19th century. Independent introductions on these three continents provide a robust system to investigate invasion genetics. In this study, we compare mitochondrial diversity in European starlings from North America, Australia, and South Africa, and a portion of the native range in the United Kingdom. Of the three invasive ranges, the North American population shows the highest haplotype diversity and evidence of both sudden demographic and spatial expansion. Comparatively, the Australian population shows the lowest haplotype diversity, but also shows evidence for sudden demographic and spatial expansion. South Africa is intermediate to the other invasive populations in genetic diversity but does not show evidence of demographic expansion. In previous studies, population genetic structure was found in Australia, but not in South Africa. Here we find no evidence of population structure in North America. Although all invasive populations share haplotypes with the native range, only one haplotype is shared between invasive populations. This suggests these three invasive populations represent independent subsamples of the native range. The structure of the haplotype network implies that the native-range sampling does not comprehensively characterize the genetic diversity there. This study represents the most geographically widespread analysis of European starling population genetics to date.

Hominoid intraspecific cranial variation mirrors neutral genetic diversity.

Natural selection, developmental constraint, and plasticity have all been invoked as explanations for intraspecific cranial variation in humans and apes. However, global patterns of human cranial variation are congruent with patterns of genetic variation, demonstrating that population history has influenced cranial variation in humans. Here we show that this finding is not unique to Homo sapiens but is also broadly evident across extant ape species. Specifically, taxa that exhibit greater intraspecific cranial shape variation also exhibit greater genetic diversity at neutral autosomal loci. Thus, cranial shape variation within hominoid taxa reflects the population history of each species. Our results suggest that neutral evolutionary processes such as mutation, gene flow, and genetic drift have played an important role in generating cranial variation within species. These findings are consistent with previous work on human cranial morphology and improve our understanding of the evolutionary processes that generate intraspecific cranial shape diversity within hominoids. This work has implications for the analysis of selective and developmental pressures on the cranium and for interpreting shape variation in fossil hominin crania.

Look in the trees: Hylobatids as evolutionary models for extinct hominins.

Studying extant apes is of central importance to paleoanthropology. This approach is informative in inferring how hominin skeletal morphology reflects phylogeny, behavior, development, and ecological context. Traditionally, great apes have dominated the paleoanthropological literature as extant analogs for extinct hominins, to the exclusion of their phylogenetic sister group, the hylobatids. Phylogenetic proximity, large body size, and high encephalization quotients may have contributed to decisions to use great apes as models for hominins. However, if we reexamine hylobatids as extant models for extinct hominins-using modern phylogenetic, behavioral, and ecological data-this clade is uniquely poised to inform future frameworks in paleoanthropology. The following features make hylobatids strong analogs for extinct hominins: taxonomic diversity, the timing of diversification, hybridization between species, small body size, and reduced sexual dimorphism. Based on these shared features, hylobatids offer future opportunities to paleoanthropology, and provide a much richer extant analog than is currently recognized.

The SLC4A1 gene is under differential selective pressure in primates infected by Plasmodium falciparum and related parasites.

Malaria is a disease caused by Plasmodium parasites and is responsible for high mortality in humans. This disease is caused by four different species of Plasmodium though the main source of mortality is Plasmodium falciparum. Humans have a number of genetic adaptations that act to combat Plasmodium. One adaptation is a deletion in the SLC4A1 gene that leads to Southeast Asian ovalocytosis (SAO). There is evidence that SAO erythrocytes are resistant to multiple Plasmodium species. Here we analyze SLC4A1 in 23 primates and mammals to test for differential selective pressures among different primate lineages. Because primates are infected with both human Plasmodium parasites and their relatives, this analysis can be used to test which human Plasmodium parasite is the likely target of SAO. A significantly different pattern of molecular evolution was found in humans and African apes, species that are infected by P. falciparum and its relatives. This effect was restricted to the cytosolic domain of the SLC4A1 gene. The evidence is consistent with a different selective regime operating on this gene domain in humans and African apes, when compared to other primates and mammals. Alternatively, this pattern is consistent with a relaxation of selection or weak adaptive evolution operating on a small number of amino acids. The adaptive interpretation of the results is consistent with the SAO allele of the SLC4A1 gene interacting with P. falciparum in humans, rather than other Plasmodium parasites. However, additional investigation of the relationship between SLC4A1 variants and Plasmodium in humans and African apes is required to test whether the different selective regime in humans and African apes is due to natural selection or relaxed constraint.

Phylogenetic analysis of the promoter region of the CD40L gene in primates and other mammals.

CD40L is a type II membrane protein comprised of 261 amino acids. CD40L plays a crucial role in the immune system where it is primarily expressed on activated T cells and triggers immunoglobulin class switching. The genetic disease X-linked hypergammaglobulinemia (HIGM1, XHIGM or XHIM) is caused by mutations in the CD40L gene. Individuals with HIGM1 are susceptible to recurrent infections to pathogens and a relationship has been shown to exist with malaria [Sabeti, P., Usen, S., Farhadian, S., Jallow, M., Doherty, T., Newport, M., Pinder, M., Ward, R., Kwiatkowski, D., 2002a. CD40L association with protection from severe malaria. Genes Immun. 3, 286-291]. In this paper, we phylogenetically examine the promoter region of CD40L in primates and other mammals via phylogenetic shadowing. This analysis revealed several regions of the CD40L promoter that were highly constrained and thereby inferred to be functional. These constrained regions confirmed many known regulatory sites. In addition, a novel, highly constrained upstream region was also identified which had an NF-AT recognition motif. These analyses also showed that the different mammal groups do not share an exactly similar set of promoter binding sites and taxon-specific promoters have evolved.