Global loss of avian evolutionary uniqueness in urban areas

Urbanization, one of the most important anthropogenic impacts on Earth, is rapidly expanding worldwide. This expansion of urban land‐covered areas is known to significantly reduce different components of biodiversity. However, the global evidence for this effect is mainly focused on a single diversity measure (species richness) with a few local or regional studies also supporting reductions in functional diversity. We have used birds, an important ecological group that has been used as surrogate for other animals, to investigate the hypothesis that urbanization reduces the global taxonomical and/or evolutionary diversity. We have also explored whether there is evidence supporting that urban bird communities are evolutionarily homogenized worldwide in comparison with nonurban ones by means of using evolutionary distinctiveness (how unique are the species) of bird communities. To our knowledge, this is the first attempt to quantify the effect of urbanization in more than one single diversity measure as well as the first time to look for associations between urbanization and phylogenetic diversity at a large spatial scale. Our findings show a strong and globally consistent reduction in taxonomic diversity in urban areas, which is also synchronized with the evolutionary homogenization of urban bird communities. Despite our general patterns, we found some regional differences in the intensity of the effect of cities on bird species richness or evolutionary distinctiveness, suggesting that conservation efforts should be adapted locally. Our findings might be useful for conservationists and policymakers to minimize the impact of urban development on Earth's biodiversity and help design more realistic conservation strategies.     

Beyond the evolutionary theory of ageing, from functional genomics to evo-gero

By the mid 1970s, the mechanisms by which ageing can evolve had a secure theoretical basis in population genetics. Here, we discuss how subsequent evolutionary work has focussed on testing and extending this theory, and on attempting to integrate it with other emerging facets of the biology of ageing, such as genetic studies of long-lived mutants and of phenotypic plasticity in ageing, such as in response to nutritional status. We also describe how functional genomic studies are providing new insights into the evolutionary forces shaping genome evolution and lifespan control. Future challenges include understanding the biochemistry of longevity and how its failure generates ageing and associated diseases, and the determination of the genetic basis of lifespan evolution and the great plasticity that it displays.     

Systems biology of ageing and longevity

Ageing is intrinsically complex, being driven by multiple causal mechanisms. Each mechanism tends to be partially supported by data indicating that it has a role in the overall cellular and molecular pathways underlying the ageing process. However, the magnitude of this role is usually modest. The systems biology approach combines (i) data-driven modelling, often using the large volumes of data generated by functional genomics technologies, and (ii) hypothesis-driven experimental studies to investigate causal pathways and identify their parameter values in an unusually quantitative manner, which enables the contributions of individual mechanisms and their interactions to be better understood, and allows for the design of experiments explicitly to test the complex predictions arising from such models. A clear example of the success of the systems biology approach in unravelling the complexity of ageing can be seen in recent studies on cell replicative senescence, revealing interactions between mitochondrial dysfunction, telomere erosion and DNA damage. An important challenge also exists in connecting the network of (random) damage-driven proximate mechanisms of ageing with the higher level (genetically specified) signalling pathways that influence longevity. This connection is informed by actions of natural selection on the determinants of ageing and longevity.     

The evolution of ageing and longevity.

Ageing is not adaptive since it reduces reproductive potential, and the argument that it evolved to provide offspring with living space is hard to sustain for most species. An alternative theory is based on the recognition that the force of natural selection declines with age, since in most environments individuals die from predation, disease or starvation. Ageing could therefore be the combined result of late-expressed deleterious genes which are beyond the reach of effective negative selection. However, this argument is circular, since the concept of 'late expression' itself implies the prior existence of adult age-related physiological processes. Organisms that do not age are essentially in a steady state in which chronologically young and old individuals are physiologically the same. In this situation the synthesis of macromolecules must be sufficiently accurate to prevent error feedback and the development of lethal 'error catastrophes'. This involves the expenditure of energy, which is required for both kinetic proof-reading and other accuracy promoting devices. It may be selectively advantageous for higher organisms to adopt an energy saving strategy of reduced accuracy in somatic cells to accelerate development and reproduction, but the consequence will be eventual deterioration and death. This 'disposable soma' theory of the evolution of ageing also proposes that a high level of accuracy is maintained in immortal germ line cells, or alternatively, that any defective germ cells are eliminated. The evolution of an increase in longevity in mammals may be due to a concomitant reduction in the rates of growth and reproduction and an increase in the accuracy of synthesis of macromolecules. The theory can be tested by measuring accuracy in germ line and somatic cells and also by comparing somatic cells from mammals with different longevities.     

Genetic support for the evolutionary theory of reproductive transactions in social wasps

Recent evolutionary models of reproductive partitioning within animal societies (known as 'optimal skew', 'concessions' or 'transactional' models) predict that a dominant individual will often yield some fraction of the group's reproduction to a subordinate as an incentive to stay in the group and help rear the dominant's offspring. These models quantitatively predict how the magnitude of the subordinate's 'staying incentive' will vary with the genetic relatedness between dominant and subordinate, the overall expected group output and the subordinate's expected output if it breeds solitarily. We report that these predictions accord remarkably well with the observed reproductive partitioning between conesting dominant and subordinate queens in the social paper wasp Polistes fuscatus. In particular, the theory correctly predicts that (i) the dominant's share of reproduction, i.e. the skew, increases as the colony cycle progresses and (ii) the skew is positively associated both with the colony's productivity and with the relatedness between dominant and subordinate. Moreover, aggression between foundresses positively correlated with the skew, as predicted by transactional but not alternative tug-of-war models of societal evolution. Thus, our results provide the strongest (quantitative support yet for a unifying model of social evolution.     

The longevity of diploid and polyploid human fibroblasts : Evidence against the somatic mutation theory of cellular ageing

Diploid human foetal lung fibroblasts, strain MRC-5, were treated with colchicine for 3 or 6 h, and the surviving population was found to contain up to 60% polyploid (mainly tetraploid) cells. The lifespan of treated cultures was not significantly different from controls. Cultures of different passage level were treated with colchicine and the proportion of polyploids was measured at intervals throughout their subsequent serial subculture until senescence and death occurred. In all cases it was found that the proportion of polyploids remained constant until the end of the lifespan. This indicates that both the growth rate and the longevity of diploids and polyploids is very similar. The results are compatible with either the protein error or programme theory of ageing and provide evidence against any mutation theory which proposes that ageing is due to the accumulation of recessive genetic defects or mutations.     

Pathophysiology of ageing, longevity and age related diseases

On April 18, 2007 an international meeting on Pathophysiology of Ageing, Longevity and Age-Related Diseases was held in Palermo, Italy. Several interesting topics on Cancer, Immunosenescence, Age-related inflammatory diseases and longevity were discussed. In this report we summarize the most important issues. However, ageing must be considered an unavoidable end point of the life history of each individual, nevertheless the increasing knowledge on ageing mechanisms, allows envisaging many different strategies to cope with, and delay it. So, a better understanding of pathophysiology of ageing and age-related disease is essential for giving everybody a reasonable chance for living a long and enjoyable final part of the life.     

Density dependence, lifespan and the evolutionary dynamics of longevity

Longevity is a life-history trait that is shaped by natural selection. Evolution will shape mortality trajectories and lifespans, but until now the evolutionary analysis of longevity is based principally on a density-independent (Euler-Lotka) framework. The effects of density dependence on the evolution of lifespan and mortality remain largely unexplored. We investigate the influence of different population demographies on the evolution of longevity, and show how these can be linked to adaptive radiations. We present a range of models to explore the intraspecific and interspecific density effects on longevity and, consequently, diversification. We show how the magnitude, type, and timing of mutation can also affect fitness, invasion and diversification. We argue that fitness of alternative strategies under a range of different demographic structures leads to flat, as opposed to rugged, landscapes and that these flat fitness surfaces are important in the evolution of lifespan and senescence.     

Further support to the uncoupling-to-survive theory: the genetic variation of human UCP genes is associated with longevity

In humans Uncoupling Proteins (UCPs) are a group of five mitochondrial inner membrane transporters with variable tissue expression, which seem to function as regulators of energy homeostasis and antioxidants. In particular, these proteins uncouple respiration from ATP production, allowing stored energy to be released as heat. Data from experimental models have previously suggested that UCPs may play an important role on aging rate and lifespan. We analyzed the genetic variability of human UCPs in cohorts of subjects ranging between 64 and 105 years of age (for a total of 598 subjects), to determine whether specific UCP variability affects human longevity. Indeed, we found that the genetic variability of UCP2, UCP3 and UCP4 do affect the individual's chances of surviving up to a very old age. This confirms the importance of energy storage, energy use and modulation of ROS production in the aging process. In addition, given the different localization of these UCPs (UCP2 is expressed in various tissues including brain, hearth and adipose tissue, while UCP3 is expressed in muscles and Brown Adipose Tissue and UCP4 is expressed in neuronal cells), our results may suggest that the uncoupling process plays an important role in modulating aging especially in muscular and nervous tissues, which are indeed very responsive to metabolic alterations and are very important in estimating health status and survival in the elderly.     

Cytogenetic perspective of ageing and longevity in men and women

Analysis of relationships between the ageing cell phenotype and the age of cell donors is one of the ways towards understanding the link between cellular and organismal ageing. Cytogenetically, ageing is associated with a number of gross cellular changes, including altered size and morphology, genomic instability, and changes in expression and proliferation. Genomic instability can be easily assessed by analyzing the level of cytogenetic aberrations. In this review, we focus on the differences in the level and profile of cytogenetic aberrations observed in donors of different age and gender. Centenarians are a small fraction of the population at the extreme of human longevity. Their inclusion in such studies may shed light on one of the basic questions: whether genome stability is better maintained in successfully aged individuals compared to the rest of the population. At the same time, comparing the profile of age-related amount of chromosomal aberrations in men and women may help explaining the commonly observed gender differences in longevity.     

Pharmacology,genomics, and the evolutionary biology of ageing

Aging is a multifold process affected by many genes and thus many biochemical pathways. This conclusion is underscored by the failure to find simple central controls for the aging process during the 20th Century. This situation poses a fundamental challenge to anti-aging medicine: how to develop effective therapies for a genomically complex pathology. We propose such a strategy. As a first step, we recommend the use of model systems in which significant genetic intervention is not proscribed or impractical. Second, we propose that work with such model systems begin with selected lines that have genetic enhancements that allow increased lifespan. Third, genomic methods should be used to identify a number of biochemical pathways for increasing lifespan. Fourth, biochemical pathways that have been identified in model systems would then be available for pharmaceutical development, first in rodents, eventually in a clinical human population. This may seem to be a cumbersome R&D strategy, but starting with human populations or inadequately pre-screened compounds would be unlikely to succeed because of the complexity of the aging problem.     

Perinatal sadness among Shuar women: support for an evolutionary theory of psychic pain

Psychiatry faces an internal contradiction in that it regards mild sadness and low mood as normal emotions, yet when these emotions are directed toward a new infant, it regards them as abnormal. We apply parental investment theory, a widely used framework from evolutionary biology, to maternal perinatal emotions, arguing that negative emotions directed toward a new infant could serve an important evolved function. If so, then under some definitions of psychiatric disorder, these emotions are not disorders. We investigate the applicability of parental investment theory to maternal postpartum emotions among Shuar mothers. Shuar mothers' conceptions of perinatal sadness closely match predictions of parental investment theory.     

Extinction as a driver of avian latitudinal diversity gradients

The role of historical factors in driving latitudinal diversity gradients is poorly understood. Here, we used an updated global phylogeny of terrestrial birds to test the role of three key historical factors—speciation, extinction, and dispersal rates—in generating latitudinal diversity gradients for eight major clades. We fit a model that allows speciation, extinction, and dispersal rates to differ, both with latitude and between the New and Old World. Our results consistently support extinction (all clades had lowest extinction where species richness was highest) as a key driver of species richness gradients across each of eight major clades. In contrast, speciation and dispersal rates showed no consistent latitudinal patterns across replicate bird clades, and thus are unlikely to represent general underlying drivers of latitudinal diversity gradients.     

Longevity and ageing: appraising the evolutionary consequences of growing old

Senescence or ageing is an increase in mortality and/or decline in fertility with increasing age. Evolutionary theories predict that ageing or longevity evolves in response to patterns of extrinsic mortality or intrinsic damage. If ageing is viewed as the outcome of the processes of behaviour, growth and reproduction then it should be possible to predict mortality rate. Recent developments have shown that it is now possible to integrate these ecological and physiological processes and predict the shape of mortality trajectories. By drawing on the key exciting developments in the cellular, physiological and ecological process of longevity the evolutionary consequences of ageing are reviewed. In presenting these ideas an evolutionary demographic framework is used to argue how trade-offs in life-history strategies are important in the maintenance of variation in longevity within and between species. Evolutionary processes associated with longevity have an important role in explaining levels of biological diversity and speciation. In particular, the effects of life-history trait trade-offs in maintaining and promoting species diversity are explored. Such trade-offs can alleviate the effects of intense competition between species and promote species coexistence and diversification. These results have important implications for understanding a number of core ecological processes such as how species are divided among niches, how closely related species co-occur and the rules by which species assemble into food-webs. Theoretical work reveals that the proximate physiological processes are as important as the ecological factors in explaining the variation in the evolution of longevity. Possible future research challenges integrating work on the evolution and mechanisms of growing old are briefly discussed.     

A theory for the evolutionary game

We present an evolutionary game theory. This theory differs in several respects from current theories related to Maynard Smith's pioneering work on evolutionary stable strategies (ESS). Most current work deals with two person matrix games. For these games the strategy set is finite. We consider evolutionary games which are defined over a continuous strategy set and which permit any number of players. Matrix games are included as a bilinear continuous game. However, under our definition, such games will not posses an ESS on the interior of the strategy set. We extend previous work on continuous games by developing an ESS definition which permits the ESS to be composed of a coalition of several strategies. This definition requires that the coalition must not only be stable with respect to perturbations in strategy frequencies which comprise the coalition, but the coalition must also satisfy the requirement that no mutant strategies can invade. Ecological processes are included in the model by explicitly considering population size and density dependent selection.     

Origin of evolutionary change in avian clutch size

Why different bird species lay different numbers of eggs is a question that has long been associated with factors external to the organism, that is, factors which operate on inherited variation in clutch size through the action of natural selection. Yet, while external factors are important, the extent of what is evolutionarily possible rests with the mechanisms developed by birds for clutch‐size control. Hitherto neglected, these mechanisms generate factors internal to the organism that are central to the origin of evolutionary change. They are related to the fact that a species‐specific range of clutch size arises from the differential survival of pre‐ovulatory follicles undergoing growth when the signal causing egg laying to end reaches the ovary. Herein, I examine three internal factors that, together with external factors, could impact the evolution of avian clutch size. Each factor acts by changing either the number of pre‐ovulatory follicles present in the ovary at the time of follicular disruption or the timing of this event. These changes to clutch size can be explained by the concept of heterochrony. In light of this, the role of phenotypic plasticity and genes determining clutch size is discussed. Finally, to account for the origin of evolutionary change in clutch size, I detail an hypothesis involving a process similar to Waddington's theory of genetic assimilation.     

Applied conservation services of the evolutionary theory

Having quantitative data to use in a reliable model in conservation can be extremely limiting because of the usual scarcity of such information. The body of theory accumulated so far in evolutionary ecology, and particularly in the evolution of life-history traits, can also come in the aid of conservation practitioners and provide them with some help in the absence of quantitative data. Although some attempts have been made already to bridge the gap between evolution and applied conservation, this interface remains to be properly delineated. Here we present a diverse number of examples of the applicability of evolutionary knowledge to the effective solution of diverse applied conservation problems. We first deal with the opposed strategies of animal and plant species inhabiting survival versus reproduction habitats, and the most adequate management approaches in both cases, with special emphasis in assessing the risks of supplementing food and nest boxes for conservation purposes. Secondly, we deal with invasion biology and suggest that a better understanding of the problem of biological invasions, and a better management of it, is gained if the focus is moved from invasive species characteristics to the properties of the invaded community from an evolutionary perspective. Finally, we show how the management of complex predator–prey interactions can benefit from the application of knowledge on life-history evolution and discuss the particularities of culling programs applied either to short-lived or long-lived species in order to be effective.