5,964 research outputs found

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

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    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

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

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    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

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    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

    Genetic noise control via protein oligomerization

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    Gene expression in a cell entails random reaction events occurring over disparate time scales. Thus, molecular noise that often results in phenotypic and population-dynamic consequences sets a fundamental limit to biochemical signaling. While there have been numerous studies correlating the architecture of cellular reaction networks with noise tolerance, only a limited effort has been made to understand the dynamic role of protein-protein interactions. Here we have developed a fully stochastic model for the positive feedback control of a single gene, as well as a pair of genes (toggle switch), integrating quantitative results from previous in vivo and in vitro studies. We find that the overall noise-level is reduced and the frequency content of the noise is dramatically shifted to the physiologically irrelevant high-frequency regime in the presence of protein dimerization. This is independent of the choice of monomer or dimer as transcription factor and persists throughout the multiple model topologies considered. For the toggle switch, we additionally find that the presence of a protein dimer, either homodimer or heterodimer, may significantly reduce its random switching rate. Hence, the dimer promotes the robust function of bistable switches by preventing the uninduced (induced) state from randomly being induced (uninduced). The specific binding between regulatory proteins provides a buffer that may prevent the propagation of fluctuations in genetic activity. The capacity of the buffer is a non-monotonic function of association-dissociation rates. Since the protein oligomerization per se does not require extra protein components to be expressed, it provides a basis for the rapid control of intrinsic or extrinsic noise

    Social environment mediates cancer progression in Drosophila

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    The influence of oncogenic phenomena on the ecology and evolution of animal species is becoming an important research topic. Similar to host–pathogen interactions, cancer negatively affects host fitness, which should lead to the selection of host control mechanisms, including behavioral traits that best minimize the proliferation of malignant cells. Social behavior is suggested to influence tumor progression. While the ecological benefits of sociality in gregarious species are widely acknowledged, only limited data are available on the role of the social environment on cancer progression. Here, we exposed adult Drosophila, with colorectal-like tumors, to different social environments. We show how subtle variations in social structure have dramatic effects on the progression of tumor growth. Finally, we reveal that flies can discriminate between individuals at different stages of tumor development and selectively choose their social environment accordingly. Our study demonstrates the reciprocal links between cancer and social interactions and how sociality may impact health and fitness in animals and its potential implications for disease ecology.This work was supported by the ANR (Blanc project EVOCAN to F.T. and project DROSONET to F.M. and C.S.), the CNRS (INEE and INSB), Fondation ARC (1555286 to J.M. and F.M.), The French league against Cancer (M27218 to J.M.), IDEEV program (to F.M.), by an International Associated Laboratory Project France/Australia, by the French-Australian Science Innovation Collaboration Program Early Career Fellowship (B.U.), by André Hoffmann (Fondation MAVA), Fyssen Foundation (to F.M. and E.H. D.) and the French Government (fellowship 2015–155 to M.D.)

    On the relationship between K concentration, grain size and dose in feldspar

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    Previous work has been unable to establish a relationship between K concentration and De in single-grains of feldspar. Here we use four well-bleached sediments with low external dose rate (typically ≤1.5 Gy ka-1) to investigate this relationship. Single and multi-grain pIRIR measurements and μ-XRF analyses are made on Na- and K-rich extracts; μ-XRF is directly applied to grains sitting in single-grain discs to minimise uncertainty in grain identification. Micro-XRF is shown to be sufficiently precise and accurate and luminescence instrument reproducibility is confirmed using dose recovery measurements on heated feldspar. We are again unable to establish any correlation between single-grain De and K concentration, even in feldspar grains for which the internal dose rate should dominate. We also measure highly variable Rb concentrations in these grains and are unable to detect, at the single-grain level, the correlation between K and Rb previously observed in multi-grain investigations. Nevertheless, these results are unable to explain the lack of De correlation with K. Finally, we investigate the dependence of De on grain size (isochrons). Linear correlations are observed but slopes are inconsistent with model prediction. We conclude that this surprising absence of the expected relationships between dose and K concentration and grain size does not arise from analytical precision, incomplete bleaching, sediment mixing or fading. It appears that we cannot measure feldspar doses in these samples as accurately as we thought

    Immunosenescence in wild animals:Meta-analysis and outlook

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    Immunosenescence, the decline in immune defense with age, is an important mortality source in elderly humans but little is known of immunosenescence in wild animals. We systematically reviewed and meta-analysed evidence for age-related changes in immunity in captive and free-living populations of wild species (321 effect sizes in 62 studies across 44 species of mammals, birds and reptiles). As in humans, senescence was more evident in adaptive (acquired) than innate immune functions. Declines were evident for cell function (antibody response), the relative abundance of naive immune cells and an in vivo measure of overall immune responsiveness (local response to phytohaemagglutinin injection). Inflammatory markers increased with age, similar to chronic inflammation associated with human immunosenescence. Comparisons across taxa and captive vs free-living animals were difficult due to lack of overlap in parameters and species measured. Most studies are cross-sectional, which yields biased estimates of age-effects when immune function co-varies with survival. We therefore suggest longitudinal sampling approaches, and highlight techniques from human cohort studies that can be incorporated into ecological research. We also identify avenues to address predictions from evolutionary theory and the contribution of immunosenescence to age-related increases in disease susceptibility and mortality

    Operational experience with the GEM detector assembly lines for the CMS forward muon upgrade

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    The CMS Collaboration has been developing large-area triple-gas electron multiplier (GEM) detectors to be installed in the muon Endcap regions of the CMS experiment in 2019 to maintain forward muon trigger and tracking performance at the High-Luminosity upgrade of the Large Hadron Collider (LHC); 10 preproduction detectors were built at CERN to commission the first assembly line and the quality controls (QCs). These were installed in the CMS detector in early 2017 and participated in the 2017 LHC run. The collaboration has prepared several additional assembly and QC lines for distributed mass production of 160 GEM detectors at various sites worldwide. In 2017, these additional production sites have optimized construction techniques and QC procedures and validated them against common specifications by constructing additional preproduction detectors. Using the specific experience from one production site as an example, we discuss how the QCs make use of independent hardware and trained personnel to ensure fast and reliable production. Preliminary results on the construction status of CMS GEM detectors are presented with details of the assembly sites involvement

    Ecological and evolutionary consequences of anticancer adaptations

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    Cellular cheating leading to cancers exists in all branches of multicellular life, favoring the evolution of adaptations to avoid or suppress malignant progression, and/or to alleviate its fitness consequences. Ecologists have until recently largely neglected the importance of cancer cells for animal ecology, presumably because they did not consider either the potential ecological or evolutionary consequences of anticancer adaptations. Here, we review the diverse ways in which the evolution of anticancer adaptations has significantly constrained several aspects of the evolutionary ecology of multicellular organisms at the cell, individual, population, species, and ecosystem levels and suggest some avenues for future research
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