Urbanization and associated environmental changes are causing global declines in vertebrate populations. In general, population declines of the magnitudes now detected should lead to reduced effective population sizes for animals living in proximity to humans and disturbed lands. This is a cause for concern because effective population sizes set the rate of genetic diversity loss due to genetic drift, the rate of increase in inbreeding and the efficiency with which selection can act on beneficial alleles. We predicted that the effects of urbanization should decrease effective population size and genetic diversity, and increase population-level genetic differentiation. To test for such patterns, we repurposed and reanalysed publicly archived genetic datasets for North American birds and mammals. After filtering, we had usable raw genotype data from 85 studies and 41 023 individuals, sampled from 1008 locations spanning 41 mammal and 25 bird species. We used census-based urban–rural designations, human population density and the Human Footprint Index as measures of urbanization and habitat disturbance. As predicted, mammals sampled in more disturbed environments had lower effective population sizes and genetic diversity, and were more genetically differentiated from those in more natural environments. There were no consistent relationships detectable for birds. This suggests that, in general, mammal populations living near humans may have less capacity to respond adaptively to further environmental changes, and be more likely to suffer from effects of inbreeding.
Chromosomal inversions are thought to play a major role in climatic adaptation. In D. melanogaster, the cosmopolitan inversion In(3R)Payne exhibits latitudinal clines on multiple continents. Since many fitness traits show similar clines, it is tempting to hypothesize that In(3R)P underlies observed clinal patterns for some of these traits. In support of this idea, previous work in Australian populations has demonstrated that In(3R)P affects body size but not development time or cold resistance. However, similar data from other clines of this inversion are largely lacking; finding parallel effects of In(3R)P across multiple clines would considerably strengthen the case for clinal selection. Here, we have analyzed the phenotypic effects of In(3R)P in populations originating from the endpoints of the latitudinal cline along the North American east coast. We measured development time, egg-to-adult survival, several size-related traits (femur and tibia length, wing area and shape), chill coma recovery, oxidative stress resistance and triglyceride content in homokaryon lines carrying In(3R)P or the standard arrangement. Our central finding is that the effects of In(3R)P along the North American cline match those observed in Australia: standard arrangement lines were larger than inverted lines, but the inversion did not influence development time or cold resistance. Similarly, In(3R)P did not affect egg-to-adult survival, oxidative stress resistance and lipid content. In(3R)P thus seems to specifically affect size traits in populations from both continents. This parallelism strongly suggests an adaptive pattern, whereby the inversion has captured alleles associated with growth regulation and clinal selection acts on size across both continents.
Urbanization and associated environmental changes are causing global declines in vertebrate populations. In general, population declines of the magnitudes now detected should lead to reduced effective population sizes for animals living in proximity to humans and disturbed lands. This is cause for concern because effective population sizes set the rate of genetic diversity loss due to genetic drift, the rate of increase in inbreeding, and the efficiency with which selection can act on beneficial alleles. We predicted that the effects of urbanization should decrease effective population size and genetic diversity, and increase population-level genetic differentiation. To test for such patterns, we repurposed and reanalyzed publicly archived genetic data sets for North American birds and mammals. After filtering, we had usable raw genotype data from 85 studies and 41,023 individuals, sampled from 1,008 locations spanning 41 mammal and 25 bird species. We used census-based urban-rural designations, human population density, and the Human Footprint Index as measures of urbanization and habitat disturbance. As predicted, mammals sampled in more disturbed environments had lower effective population sizes and genetic diversity, and were more genetically differentiated from those in more natural environments. There were no consistent relationships detectable for birds. This suggests that, in general, mammal populations living near humans may have less capacity to respond adaptively to further environmental changes, and be more likely to suffer from effects of inbreeding.
As urban areas continue to grow, understanding how species respond and adapt to urban habitats is becoming increasingly important. Knowledge of the mechanisms behind observed phenotypic changes of urban-dwelling animals will enable us to better evaluate the impact of urbanization on current and future generations of wildlife and predict how animals respond to novel environments. Recently, urban ecology has emerged not only as a means of understanding organismal adaptation but also as a framework for exploring mechanisms mediating evolutionary phenomena. Here, we have identified four important research topics that will advance the field of urban ecology and shed light on the proximate and ultimate causes of the phenotypic differences commonly seen among species and populations that vary in their responses to urbanization. First, we address the ecological and socio-economic factors that characterize cities, how they might interact with each other, and how they affect urban species. Second, we ask which are the proximate mechanisms underlying the emergence over time of novel traits in urban organisms, focusing on developmental effects. Third, we emphasize the importance of understanding the ultimate causations that link phenotypic shifts to function. This question highlights the need to quantify the strength and direction of selection that urban individuals are exposed to, and whether the phenotypic shifts associated with life in the city are adaptive. Lastly, we stress the need to translate how individual-level responses scale up to population dynamics. Understanding the mechanistic underpinnings of variation among populations and species in their responses to urbanization will unravel species resilience to environmental perturbation, which will facilitate predictive models for sustainability and development of green cities that maintain or even increase urban biodiversity and wildlife health and wellbeing.
The processes that give rise to species richness gradients are not well understood, but may be linked to resource-based limits on the number of species a region can support. Ecological limits placed on regional species richness would also limit population sizes, suggesting that these processes could also generate genetic diversity gradients. If true, we might better understand how broad-scale biodiversity patterns are formed by identifying the common causes of genetic diversity and species richness. We develop a hypothetical framework based on the consequences of regional variation in ecological limits to simultaneously explain spatial patterns of species richness and neutral genetic diversity. Repurposing raw genotypic data spanning 38 mammal species sampled across 801 sites in North America, we show that estimates of genome-wide genetic diversity and species richness share spatial structure. Notably, species richness hotspots tend to harbor lower levels of within-species genetic variation. A structural equation model encompassing eco-evolutionary processes related to resource availability, habitat heterogeneity, and human disturbance explained 78% of variation in genetic diversity and 74% of the variation in species richness. These results suggest we can infer broad-scale patterns of species and genetic diversity using two simple environmental measures of resource availability and ecological opportunity.
Human land transformation is one of the leading causes of vertebrate population declines. These declines are thought to be partly due to decreased connectivity and habitat loss reducing animal population sizes in disturbed habitats. With time, this can lead to declines in effective population size and genetic diversity which restrict the ability of wildlife to efficiently cope with environmental change through genetic adaptation. However, it is not well understood whether these effects generally hold across taxa. We address this question by repurposing and synthesizing raw microsatellite data from online repositories for 19 amphibian species sampled at 554 georeferenced sites in North America. For each site, we estimated gene diversity, allelic richness, effective population size, and population differentiation. Using binary urban‐rural census designations, and continuous measures of human population density, the Human Footprint Index, and impervious surface cover, we tested for generalizable effects of human land use on amphibian genetic diversity. We found minimal evidence, either positive or negative, for relationships between genetic metrics and urbanization. Together with previous work on focal species that also found varying effects of urbanization on genetic composition, it seems likely that the consequences of urbanization are not easily generalizable within or across amphibian species. Questions about the genetic consequences of urbanization for amphibians should be addressed on a case‐by‐case basis. This contrasts with general negative effects of urbanization in mammals and consistent, but species‐specific, positive and negative effects in birds.
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