The potential demise of a population of adders (Vipera berus) in Smygehuk, Sweden

Abstract.—In 1999 and 2004, we published reports on how the introduction of 20 males into a severely inbred and isolated population of Adders halted its decline towards extinction. The introduction significantly enhanced the population’s genetic variability, which resulted in a dramatic increase in offspring viability and a rapid increase in numbers

How well do predators adjust to climate-mediated shifts in prey distribution? A study on Australian water pythons

Climate change can move the spatial location of resources critical for population viability, and a species resilience to such changes will depend upon its ability to flexibly shift its activities away from no-longer-suitable sites to exploit new opportunities. Intuition suggests that vagile predators should be able to track spatial shifts in prey availability, but our data on water pythons (Liasis fuscus) in tropical Australia suggest a less encouraging scenario. These pythons undergo regular long-range (to .10 km) seasonal migrations to follow flooding-induced migrations by their prey (native dusky rats, Rattus colletti ). However, when an extreme flooding event virtually eliminated rats for a three-year period, the local pythons did not disperse despite the presence of abundant rats only 8 km away; instead, many pythons starved to death. This inflexibility suggests that some vagile species that track seasonally migrating prey may do so by responding to habitat attributes that have consistently predicted prey availability over evolutionary time, rather than reacting to proximate cues that signal the presence of prey per se. A species vulnerability to climate change will be increased by an inability to shift its activities away from historical sites toward newly favorable areas. 2011 by the Ecological Society of America

A novel perspective suggesting high sustained energy expenditure may be net protective against cancer

Energy expenditure (EE) is generally viewed as tumorigenic, due to production of reactive oxygen species (ROS) that can damage cells and DNA. On this basis, individuals within a species that sustain high EE should be more likely to develop cancer. Here, we argue the opposite, that high EE may be net protective effect against cancer, despite high ROS production. This is possible because individuals that sustain high EE have a greater energetic capacity (=greater energy acquisition, expenditure and ability to up-regulate output), and can therefore allocate energy to multiple cancer-fighting mechanisms with minimal energetic trade-offs. Our review finds that individuals sustaining high EE have greater antioxidant production, lower oxidative stress, greater immune function and lower cancer incidence. Our hypothesis and literature review suggest that EE may indeed be net protective against cancer, and that individual variation in energetic capacity may be a key mechanism to understand the highly individual nature of cancer risk in contemporary human populations and laboratory animals. Lay summary The process of expending energy generates reactive oxygen species that can lead to oxidative stress, cell and DNA damage, and the accumulation of this damage is thought to be a major contributor to many ageing related diseases that include cancer. Here, we challenge this view, proposing how and why high energy expenditure (EE) may actually be net protective against cancer, and provide literature support for our hypothesis. We find individuals with high sustained EE have greater energetic capacity and thus can invest more in repair to counter oxidative stress, and more in immune function, both of which reduce cancer risk. Our hypothesis provides a novel mechanism to understand the highly individual nature of cancer, why taller individuals are more at risk, why physically active individuals have lower cancer risk, and why regular exercise can reduce cancer risk

Does mate guarding prevent rival mating in snow skinks? A test using AFLP

We report on likely mixed paternity in a natural population of snow skinks (Niveoscincus mirolepidoms) from alpine Tasmania, Australia. This species is nonterritorial and males guard females after copulation, Suggesting that guarding behavior has evolved to prevent rival mating of still-receptive females. To what degree does this mate-guarding prevent rival copulations? We sampled gravid females at random in the wild and looked for within-clutch mixed paternity among their offspring using amplified fragment length polymorphism (AFLP). Incorpating all visualized fragments, offspring band-sharing based on maternal bands was 0.94 (+/- 0.05, SD), whereas for paternal fragments it was 0.54 (+/- 0.46, SD). We then tested paternal band-sharing scores for all young of pairs against the mean score of the maternally inherited fragments to assess whether paternal genetic variation was larger than for a known single parent, hence, suggesting multiple sires. To reduce the risk of unequal sampling of polymorphic maternal and paternal fragments, We based Our statistical tests on heterozygous bands only. Offspring band sharing based on maternal heterozygous fragments was on average 0.68 ( +/- 0.22, SD), versus 0.35 (+/- 0.33, SD) based on paternally inherited fragments. in six of eight clutches (75%), at least one pair of voting in a clutch had paternal scores outside of the confidence interval for a single parent (i.e., the mother). Thus, mixed paternity seems to be widespread in this Population, despite prolonged postcopulatory mate-guarding by males

Transmissible cancers, are they more common than thought?

International audienc

Differences in mutational processes and intratumour heterogeneity between organs: the local selective filter hypothesis.

International audienceExtensive diversity (genetic, cytogenetic, epigenetic and phenotypic) exists within and between tumors, but reasons behind these variations, as well as their consistent hierarchical pattern between organs, are poorly understood at the moment. We argue that these phenomena are, at least partially, explanable by the evolutionary ecology of organs’ theory, in the same way that environmental adversity shapes mutation rates and level of polymophism in organisms. Organs in organisms can be considered as specialized ecosystems that are, for ecological and evolutionary reasons, more or less efficient at supressing tumours. When a malignancy does arise in an organ applying strong selection pressure on tumours, its constituent cells are expected to display a large range of possible surviving strategies, from hyper mutator phenotypes relying on bet-hedging to persist (high mutation rates and high diversity), to few poorly variable variants that become invisible to natural defences. In contrast, when tumour suppression is weaker, selective pressure favouring extreme surviving strategies is relaxed, and tumours are moderately variable as a result. We provide a comprehensive overview of this hypothesis

Telomere dynamics and homeostasis in a transmissible cancer

Devil Facial Tumour Disease (DFTD) is a unique clonal cancer that threatens the world\u27s largest carnivorous marsupial, the Tasmanian devil (Sarcophilus harrisii) with extinction. This transmissible cancer is passed between individual devils by cell implantation during social interactions. The tumour arose in a Schwann cell of a single devil over 15 years ago and since then has expanded clonally, without showing signs of replicative senescence; in stark contrast to a somatic cell that displays a finite capacity for replication, known as the “Hayflick limit”

In vitro competition between two transmissible cancers and potential implications for their host, the Tasmanian devil

Since the emergence of a transmissible cancer, devil facial tumour disease (DFT1), in the 1980s, wild Tasmanian devil populations have been in decline. In 2016, a second, independently evolved transmissible cancer (DFT2) was discovered raising concerns for survival of the host species. Here, we applied experimental and modelling frameworks to examine competition dynamics between the two transmissible cancers in vitro. Using representative cell lines for DFT1 and DFT2, we have found that in monoculture, DFT2 grows twice as fast as DFT1 but reaches lower maximum cell densities. Using co-cultures, we demonstrate that DFT2 outcompetes DFT1: the number of DFT1 cells decreasing over time, never reaching exponential growth. This phenomenon could not be replicated when cells were grown separated by a semi-permeable membrane, consistent with exertion of mechanical stress on DFT1 cells by DFT2. A logistic model and a Lotka-Volterra competition model were used to interrogate monoculture and co-culture growth curves, respectively, suggesting DFT2 is a better competitor than DFT1, but also showing that competition outcomes might depend on the initial number of cells, at least in the laboratory. We provide theories how the in vitro results could be translated to observations in the wild and propose that these results may indicate that although DFT2 is currently in a smaller geographic area than DFT1, it could have the potential to outcompete DFT1. Furthermore, we provide a framework for improving the parameterization of epidemiological models applied to these cancer lineages, which will inform future disease management.</p

The ecology and evolution of wildlife cancers: Applications for management and conservation

Evolutionary Applications published by John Wiley &amp; Sons Ltd Ecological and evolutionary concepts have been widely adopted to understand host&ndash;pathogen dynamics, and more recently, integrated into wildlife disease management. Cancer is a ubiquitous disease that affects most metazoan species; however, the role of oncogenic phenomena in eco-evolutionary processes and its implications for wildlife management and conservation remains undeveloped. Despite the pervasive nature of cancer across taxa, our ability to detect its occurrence, progression and prevalence in wildlife populations is constrained due to logistic and diagnostic limitations, which suggests that most cancers in the wild are unreported and understudied. Nevertheless, an increasing number of virus-associated and directly transmissible cancers in terrestrial and aquatic environments have been detected. Furthermore, anthropogenic activities and sudden environmental changes are increasingly associated with cancer incidence in wildlife. This highlights the need to upscale surveillance efforts, collection of critical data and developing novel approaches for studying the emergence and evolution of cancers in the wild. Here, we discuss the relevance of malignant cells as important agents of selection and offer a holistic framework to understand the interplay of ecological, epidemiological and evolutionary dynamics of cancer in wildlife. We use a directly transmissible cancer (devil facial tumour disease) as a model system to reveal the potential evolutionary dynamics and broader ecological effects of cancer epidemics in wildlife. We provide further examples of tumour&ndash;host interactions and trade-offs that may lead to changes in life histories, and epidemiological and population dynamics. Within this framework, we explore immunological strategies at the individual level as well as transgenerational adaptations at the population level. Then, we highlight the need to integrate multiple disciplines to undertake comparative cancer research at the human&ndash;domestic&ndash;wildlife interface and their environments. Finally, we suggest strategies for screening cancer incidence in wildlife and discuss how to integrate ecological and evolutionary concepts in the management of current and future cancer epizootics

Darwin, the devil, and the management of transmissible cancers

Modern conservation science frequently relies on genetic tools to manage imperiled populations threatened by processes such as habitat fragmentation and infectious diseases. Translocation of individuals to restore genetic diversity (genetic rescue) is increasingly used to manage vulnerable populations, but it can swamp local adaptations and lead to outbreeding depression. Thus, genetic management is context dependent and needs evaluation across multiple generations . Genomic studies can help evaluate the extent to which populations are locally adapted to assess the costs and benefits of translocations. Predicting the long‐term fitness effects of genetic interventions and their evolutionary consequences is a vital step in managing dwindling populations threatened by emerging infectious diseases