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570 results for “Exposure data”
Data from: Exposure to dairy manure leads to greater antibiotic resistance and increased mass-specific respiration in soil microbial communities
Intensifying livestock production to meet the demands of a growing global population coincides with increases in both the administration of veterinary antibiotics and manure inputs to soils. These trends have the potential to increase antibiotic resistance in soil microbial communities. The effect of maintaining increased antibiotic resistance on soil microbial communities and the ecosystem processes they regulate is unknown. We compare soil microbial communities from paired reference and dairy manure-exposed sites across the USA. Given that manure exposure has been shown to elicit increased antibiotic resistance in soil microbial communities, we expect that manure-exposed sites will exhibit (i) compositionally different soil microbial communities, with shifts toward taxa known to exhibit resistance; (ii) greater abundance of antibiotic resistance genes; and (iii) corresponding maintenance of antibiotic resistance would lead to decreased microbial efficiency. We found that bacterial and fungal communities differed between reference and manure-exposed sites. Additionally, the β-lactam resistance gene ampC was 5.2-fold greater under manure exposure, potentially due to the use of cephalosporin antibiotics in dairy herds. Finally, ampC abundance was positively correlated with indicators of microbial stress, and microbial mass-specific respiration, which increased 2.1-fold under manure exposure. These findings demonstrate that the maintenance of antibiotic resistance associated with manure inputs alters soil microbial communities and ecosystem function.
Data from: Early life exposure to low levels of AHR agonist PCB126 (3,3',4,4',5-pentachlorobiphenyl) reprograms gene expression in adult brain
Early life exposure to environmental chemicals can have long-term consequences that are not always apparent until later in life. We recently demonstrated that developmental exposure of zebrafish to low, non-embryotoxic levels of 3,3',4,4',5-pentachlorobiphenyl (PCB126) did not affect larval behavior, but caused changes in adult behavior. The objective of this study was to investigate the underlying molecular basis for adult behavioral phenotypes resulting from early life exposure to PCB126. We exposed zebrafish embryos to PCB126 during early development and measured transcriptional profiles in whole embryos, larvae and adult male brains using RNA-sequencing. Early life exposure to 0.3 nM PCB126 induced cyp1a transcript levels in 2-dpf embryos, but not in 5-dpf larvae, suggesting transient activation of aryl hydrocarbon receptor with this treatment. No significant induction of cyp1a was observed in the brains of adults exposed as embryos to PCB126. However, a total of 2209 and 1628 genes were differentially expressed in 0.3 nM and 1.2 nM PCB126-exposed groups, respectively. KEGG pathway analyses of upregulated genes in the brain suggest enrichment of calcium signaling, MAPK and notch signaling, and lysine degradation pathways. Calcium is an important signaling molecule in the brain and altered calcium homeostasis could affect neurobehavior. The downregulated genes in the brain were enriched with oxidative phosphorylation and various metabolic pathways, suggesting that the metabolic capacity of the brain is impaired. Overall, our results suggest that PCB exposure during sensitive periods of early development alters normal development of the brain by reprogramming gene expression patterns, which may result in alterations in adult behavior.
Data from: Cold adaptation increases rates of nutrient flow and metabolic plasticity during cold exposure in Drosophila melanogaster
Metabolic flexibility is an important component of adaptation to stressful environments, including thermal stress and latitudinal adaptation. A long history of population genetic studies suggest that selection on core metabolic enzymes may shape life histories by altering metabolic flux. However, the direct relationship between selection on thermal stress hardiness and metabolic flux has not previously been tested. We investigated flexibility of nutrient catabolism during cold stress in Drosophila melanogaster artificially selected for fast or slow recovery from chill coma (i.e. cold-hardy or -susceptible), specifically testing the hypothesis that stress adaptation increases metabolic turnover. Using 13C-labelled glucose, we first showed that cold-hardy flies more rapidly incorporate ingested carbon into amino acids and newly synthesized glucose, permitting rapid synthesis of proline, a compound shown elsewhere to improve survival of cold stress. Second, using glucose and leucine tracers we showed that cold-hardy flies had higher oxidation rates than cold-susceptible flies before cold exposure, similar oxidation rates during cold exposure, and returned to higher oxidation rates during recovery. Additionally, cold-hardy flies transferred compounds among body pools more rapidly during cold exposure and recovery. Increased metabolic turnover may allow cold-adapted flies to better prepare for, resist and repair/tolerate cold damage. This work illustrates for the first time differences in nutrient fluxes associated with cold adaptation, suggesting that metabolic costs associated with cold hardiness could invoke resource-based trade-offs that shape life histories.
Data from: Predator exposure improves anti-predator responses in a threatened mammal
Incorporating an understanding of animal behaviour into conservation programmes can influence conservation outcomes. Exotic predators can have devastating impacts on native prey species and thwart reintroduction efforts, in part due to prey naïveté caused by an absence of co-evolution between predators and prey. Attempts have been made to improve the anti-predator behaviours of reintroduced native prey by conducting laboratory-based predator recognition training but results have been varied and have rarely led to improved survival in reintroduction programmes. We investigated whether in situ predator exposure could improve anti-predator responses of a predator-naïve mammal by exposing prey populations to low densities of introduced predators under controlled conditions. We reintroduced 352 burrowing bettongs to a 26-km2 fenced exclosure at the Arid Recovery Reserve in South Australia and exposed them to feral cats (density 0.03–0.15 cats/km2) over an 18-month period. At the same time, we translocated a different group of bettongs into an exclosure free of introduced predators, as a control. We compared three behaviours (flight initiation distances, trap docility and behaviour at feeding trays) of cat-exposed and control bettongs before the translocations, then at 6, 12 and 18 months post-translocation. Cat-exposed bettongs displayed changes in behaviour that suggested increased wariness, relative to control bettongs. At 18 months post-reintroduction, cat-exposed bettongs had greater flight initiation distances and approached feed trays more slowly than control bettongs. Cat-exposed bettongs also increased their trap docility over time. Synthesis and applications. Translocation is recommended as a conservation tool for many threatened species yet success rates are generally low. We demonstrate that controlled levels of in situ predator exposure can increase wariness in the behaviour of naïve prey. Our findings provide support for the hypothesis that in situ predator exposure could be used as a method to improve the anti-predator responses of predator-naïve threatened species populations.
Data from: Parental exposure modulates the effects of UV-B on offspring in guppies
1.The environment experienced by parents can alter offspring phenotypes. Such developmental plasticity is beneficial when it optimises offspring responses to their prevailing environment. Plasticity may be detrimental, however, if there is a mismatch between parental and offspring environments, although reversible acclimation within individuals could counteract a developmental mismatch. 2.UV-B radiation damages cells directly and by increasing reactive oxygen species (ROS) formation. There are indications that the developmental environment can influence ROS defences, which could enhance performance and fitness. Additionally, animals exposed to UV-B can acclimate to increase their antioxidant defences and thereby reduce ROS-induced damage. Our aim was to test experimentally whether there are transgenerational effects of UV-B exposure. We tested the hypothesis that parental exposure to UV-B modulates offspring ROS defence mechanisms to reduce the negative effects of UV-B in offspring. 3.In a fully factorial experiment, we show that exposing guppies (Poecilia reticulata) to UV-B increased the resilience of their offspring to the negative effects of UV-B. When exposed to UV-B, offspring from parents also exposed to UV-B had significantly greater sustained swimming performance compared to controls. Higher swimming performance was paralleled by increased catalase activity and glutathione concentrations, and reduced ROS-induced damage to membranes and proteins. There was no effect of parental exposure to UV-B on offspring superoxide dismutase activity, resting and active metabolic rates, or offspring size. However, parental exposure to UV-B increased damage to proteins and infection rates by white spot fungus in control (no UV-B) offspring. 4.Our results showed that UV-B acts as a signal that can induce developmental modification of phenotypes. Transgenerational matching of offspring phenotypes is likely to have a fitness advantage in environments exposed to UV-B. However, the trade-off between the beneficial effects of parental UV-B exposure on offspring performance when exposed to UV-B, and the increased susceptibility to infection and protein damage when offspring are not exposed to UV-B can be important in determining the resilience of populations in variable and modified environments.
Data from: Cell death and survival due to cytotoxic exposure modeled as a two-state Ising system
<p>Cancer chemotherapy agents are assessed for their therapeutic utility primarily by their ability to cause apoptosis of cancer cells and their potency is given by an IC50 value. Chemotherapy uses both target-specific and systemic-action drugs and drug combinations to treat cancer. It is important to judiciously choose a drug type, its dosage, and schedule for optimized drug selection and administration. Consequently, the precise mathematical formulation of cancer cells response to chemotherapy may assist in the selection process. In this paper, we propose a mathematical description of the cancer cell response to chemotherapeutic agent exposure based on a time-tested physical model of two-state multiple-component systems near criticality. We describe the Ising model methodology and apply it to a diverse panel of cytotoxic drugs administered against numerous cancer cell lines in a dose-response manner. The analyzed dataset was generated by the Netherlands Translational Research Center B.V.(Oncolines). This approach allows for an accurate and consistent analysis of cytotoxic agents' effects on cancer cell lines and reveals the presence or absence of the bystander effect through the interaction constant. By calculating the susceptibility function, we see the value of IC50 coinciding with the peak of this measure of the system's sensitivity to external perturbations.</p>
Data from: Development of a genotype-by-sequencing immunogenetic assay as exemplified by screening for variation in red fox with and without endemic rabies exposure
Pathogens are recognized as major drivers of local adaptation in wildlife systems. By determining which gene variants are favored in local interactions among populations with and without disease, spatially explicit adaptive responses to pathogens can be elucidated. Much of our current understanding of host responses to disease comes from a small number of genes associated with an immune response. High-throughput sequencing (HTS) technologies, such as genotype-by-sequencing (GBS), facilitate expanded explorations of genomic variation among populations. Hybridization-based GBS techniques can be leveraged in systems not well characterized for specific variants associated with disease outcome to "capture" specific genes and regulatory regions known to influence expression and disease outcome. We developed a multiplexed, sequence capture assay for red foxes to simultaneously assess ~300-kbp of genomic sequence from 116 adaptive, intrinsic, and innate immunity genes of predicted adaptive significance and their putative upstream regulatory regions along with 23 neutral microsatellite regions to control for demographic effects. The assay was applied to 45 fox DNA samples from Alaska, where three arctic rabies strains are geographically restricted and endemic to coastal tundra regions, yet absent from the boreal interior. The assay provided 61.5% on-target enrichment with relatively even sequence coverage across all targeted loci and samples (mean = 50×), which allowed us to elucidate genetic variation across introns, exons, and potential regulatory regions (4,819 SNPs). Challenges remained in accurately describing microsatellite variation using this technique; however, longer-read HTS technologies should overcome these issues. We used these data to conduct preliminary analyses and detected genetic structure in a subset of red fox immune-related genes between regions with and without endemic arctic rabies. This assay provides a template to assess immunogenetic variation in wildlife disease systems.
Data from: Developmental exposure to PCB153 (2,2',4,4',5,5'-hexachlorobiphenyl) alters circadian rhythms and the expression of clock and metabolic genes
Polychlorinated biphenyls (PCBs) are highly persistent and ubiquitously distributed environmental pollutants. Based on their chemical structure, PCBs are classified into non-ortho-substituted and ortho-substituted congeners. Ortho-substituted PCBs are structurally similar to dioxin and their toxic effects and mode of action are well established. In contrast, very little is known about the effects of non-ortho-substituted PCBs, particularly during early development. The objective of this study is to investigate the effects of exposure to an environmentally prominent ortho-substituted PCB (2,2',4,4',5,5'-hexachlorobiphenyl; PCB153) on zebrafish embryos. We exposed zebrafish embryos to either DMSO or three different concentrations of PCB153 starting from 4 hours post-fertilization (hpf) to 120 hpf. We quantified gross morphological changes, behavioral phenotypes, gene expression changes and circadian behavior in the larvae. There were no developmental defects during the exposure period, but starting at 7 dpf, we observed spinal deformity in the 10 μM PCB153 treated group. A total of 633, 2227, and 3378 differentially expressed genes were observed in 0.1, 1 and 10 μM PCB153 treated embryos, respectively. Of these, 301 genes were common to all treatment groups. KEGG pathway analysis revealed enrichment of genes related to circadian rhythm, FoxO signaling and insulin resistance pathways. Behavioral analysis revealed that PCB153 exposure significantly alters circadian behavior. Disruption of circadian rhythms has been associated with the development of metabolic and neurological diseases. Thus, understanding the mechanisms of action on environmental chemicals in disrupting circadian regulation of metabolism is essential for preventing or mitigating chemical-induced metabolic disease.
Data from: Early-life disease exposure and associations with adult survival, cause of death, and reproductive success in preindustrial humans
A leading hypothesis proposes that increased human life span since 1850 has resulted from decreased exposure to childhood infections, which has reduced chronic inflammation and later-life mortality rates, particularly from cardiovascular disease, stroke, and cancer. Early-life cohort mortality rate often predicts later-life survival in humans, but such associations could arise from factors other than disease exposure. Additionally, the impact of early-life disease exposure on reproduction remains unknown, and thus previous work ignores a major component of fitness through which selection acts upon life-history strategy. We collected data from seven 18th- and 19th-century Finnish populations experiencing naturally varying mortality and fertility levels. We quantified early-life disease exposure as the detrended child mortality rate from infectious diseases during an individual's first 5 y, controlling for important social factors. We found no support for an association between early-life disease exposure and all-cause mortality risk after age 15 or 50. We also found no link between early-life disease exposure and probability of death specifically from cardiovascular disease, stroke, or cancer. Independent of survival, there was no evidence to support associations between early-life disease exposure and any of several aspects of reproductive performance, including lifetime reproductive success and age at first birth, in either males or females. Our results do not support the prevailing assertion that exposure to infectious diseases in early life has long-lasting associations with later-life all-cause mortality risk or mortality putatively linked to chronic inflammation. Variation in adulthood conditions could therefore be the most likely source of recent increases in adult life span.
Data from: How to characterize chemical exposure to predict ecologic effects on aquatic communities?
Reliable characterization of exposure is indispensable for ecological risk assessment of chemicals. To deal with mixtures, several approaches have been developed, but their relevance for predicting ecological effects on communities in the field has not been elucidated. In the present study, we compared nine metrics designed for estimating the total toxicity of mixtures regarding their relationship with an effect metric for stream macroinvertebrates. This was done using monitoring data of biota and organic chemicals, mainly pesticides, from five studies comprising 102 streams in several regions of Europe and South-East Australia. Mixtures of less than 10 pesticides per water sample were most common for concurrent exposure. Exposure metrics based on the 5% fraction of a species sensitivity distribution performed best, closely followed by metrics based on the most sensitive species and Daphnia magna as benchmark. Considering only the compound with the highest toxicity and ignoring mixture toxicity was sufficient to estimate toxicity in predominantly agricultural regions with pesticide exposure. The multisubstance Potentially Affected Fraction (msPAF) that combines concentration and response addition was advantageous in the study where further organic toxicants occurred. We give recommendations on exposure metric selection depending on data availability and the involved compounds.
Data from: Experimental evolution of response to anoxia in Drosophila: recovery of locomotion following CO2 or N2 exposure
Many insects enter coma upon exposure to anoxia, a feature routinely exploited by experimentalists to handle them. But the genetic and physiological bases of anoxic coma induction and recovery are only partially understood, as are the long-term consequences for the animal's performance. We examined three populations of Drosophila melanogaster (designated B) that have been inadvertently under selection for rapid recovery from CO2 exposure for nearly 40 years (around 1,000 generations) resulting from routine maintenance practices. We contrasted CO2 and N2 (presumed a less reactive gas) knockdown and recovery times of these B flies with six populations of common ancestry (A and C populations) that were not exposed to CO2 over the same period. We found that B populations showed faster and more consistent locomotor recovery than A or C populations after CO2 knockdown, a result also observed with N2 knockdown. A and C populations showed much higher variance in recovery time after CO2 exposure than after N2 exposure, suggesting gas-specific effects on pathways associated with locomotor recovery. While these selection treatments result in considerable variation in life history attributes and body size, with the characteristic intermediacy of B populations, their superiority in resistance to gas exposure and locomotor recovery suggests that it is a direct consequence of prior repeated exposure to anoxia, broadly, and CO2, specifically. Hence we describe a powerful new evolutionary model for the genetic and physiological investigation of anoxic coma in insects.
Data from: Highway to the danger zone: exposure-dependent costs of immunity in a vertebrate ectotherm
Parasite exposure often causes innate immune activation, resulting in tradeoffs among physiological processes and strong selection on the parasite. Costs of immune activation vary widely among and within host populations though, likely dependent on the evolutionary history of host-parasite interactions and the environments in which they occur. For hosts, degree of exposure may drive the magnitude of costs incurred, and subsequently whether hosts resist or tolerate infections. If costs increase concomitantly with exposure, a threshold may exist where the expense of parasite resistance becomes prohibitive and parasite tolerance becomes favorable. Here, we characterized exposure-dependent costs of an innate immune response in brown anoles (Anolis sagrei) by tracking allocation of an isotopically-labelled essential amino acid (13C-leucine), to the liver and gonads. To elicit immune responses, we used lipopolysaccharide (LPS), a strongly immunogenic molecule from Salmonella spp. We found that both sexes paid dose-dependent costs of Salmonella LPS-induced immune activation, but costs were experienced differently by the sexes, likely due to differences in life history. Males allocated more leucine to their livers in response to higher LPS doses. In females, a tendency for increased costs in response to dose were only revealed when leucine allocation ratios between lymphoid and reproductive organs were considered. We also found that regardless of dose, males always allocated more leucine to their gonads than females. Lastly, and perhaps most interestingly, cost functions in both sexes were linear, but with shallow slopes, indicating modest costs of immune activation in response to Salmonella LPS in this species. Altogether, our results demonstrate that costs of immunity are dose-dependent in this introduced lizard species, but sexes experience costs differently. Characterization of relationships between host exposure and cost of immune activation such as these can facilitate predictions about how parasites might circulate through communities.
Data from: Maternal exposure to predator scents: offspring phenotypic adjustment and dispersal
Predation is a strong selective pressure generating morphological, physiological and behavioural responses in organisms. As predation risk is often higher during juvenile stages, antipredator defences expressed early in life are paramount to survival. Maternal effects are an efficient pathway to produce such defences. We investigated whether maternal exposure to predator cues during gestation affected juvenile morphology, behaviour and dispersal in common lizards (Zootoca vivipara). We exposed 21 gravid females to saurophagous snake cues for one month while 21 females remained unexposed (i.e. control). We measured body size, preferred temperature and activity level for each neonate, and released them into semi-natural enclosures connected to corridors in order to measure dispersal. Offspring from exposed mothers grew longer tails, selected lower temperatures and dispersed thrice more than offspring from unexposed mothers. Because both tail autotomy and altered thermoregulatory behaviour are common antipredator tactics in lizards, these results suggest that mothers adjusted offspring phenotype to risky natal environments (tail length) or increased risk avoidance (dispersal). Although maternal effects can be passive consequences of maternal stress, our results strongly militate for them to be an adaptive antipredator response that may increase offspring survival prospects.
Data from: Personality and plasticity in neophobia levels vary with anthropogenic disturbance but not toxic metal exposure in urban great tits: urban disturbance, metal pollution and neophobia
Animal personalities, as defined by repeatable among individual differences in behavior, can vary across urbanization gradients. However, how urbanization affects personalities remains incompletely understood, especially because different urban stressors could affect personality traits in opposing ways, whereas most previous studies have considered only one urban disturbance factor. For instance, novel habitat features could favor reduced neophobia, whereas exposure to pollutants could increase risk sensitivity through neurotoxic or hormonal effects. To address this contingency, we studied object neophobia in four urban populations of great tits (Parus major) that vary in exposure to metal pollution and anthropogenic disturbance, as quantified by proximity to roads and pathways. We measured the return latency of incubating females when flushed from the nest and presented with up to two different novel objects, allowing quantification of behavioral repeatability and plasticity. To separate neophobia from sensitivity to disturbance, we also conducted baseline trials, in which females were flushed but no object was presented. We additionally measured exploration behavior and aggression (hissing) during nest defense, to explore whether suites of behaviors covary with urbanization, and examined whether neophobia affects reproductive success. Sensitivity to disturbance and neophobia were repeatable, and thus represent personality traits. Moreover, females occupying territories near roads and pathways had shorter return latencies during novel object but not baseline trials, suggesting a specific reduction in neophobia in disturbed areas. Plasticity in neophobia also increased with disturbance level. In contrast, metal exposure did not affect neophobia or sensitivity to disturbance, despite negatively correlating with exploration behavior. Neophobia correlated with exploration behavior, but not aggression or reproductive success. Results suggest that shifts in personality types in urbanized areas might involve specific reductions in neophobia, rather than general reductions in sensitivity to disturbance, and unexpectedly indicate no effect of toxic metals on risk sensitivity.
Data from: Variation in chronic radiation exposure does not drive life history divergence among Daphnia populations across the Chernobyl Exclusion Zone
Ionising radiation is a mutagen with known negative impacts on individual fitness. However, much less is known about how these individual fitness effects translate into population-level variation in natural environments that have experienced varying levels of radiation exposure. In this study, we sampled genotypes of the freshwater crustacean, Daphnia pulex, from the eight inhabited lakes across the Chernobyl Exclusion Zone (CEZ). Each lake has experienced very different levels of chronic radiation exposure since a nuclear power reactor exploded there over thirty years ago. The sampled Daphnia genotypes represent genetic snapshots of current populations and allowed us to examine fitness-related traits under controlled laboratory conditions at UK background dose rates. We found that whilst there was variation in survival and schedules of reproduction among populations, there was no compelling evidence that this was driven by variation in exposure to radiation. Previous studies have shown that controlled exposure to radiation at dose rates included in the range measured in the current study reduce survival, or fecundity, or both. One limitation of this study is the lack of available sites at high dose rates, and future work could test life history variation in various organisms at other high radiation areas. Our results are nevertheless consistent with the idea that other ecological factors, e.g., competition, predation or parasitism, are likely to play a much bigger role in driving variation among populations than exposure to the high radiation dose rates found in the CEZ. These findings clearly demonstrate that it is important to examine the potential negative effects of radiation across wild populations that are subject to many and varied selection pressures as a result of complex ecological interactions.
Data from: Elevated mitochondrial genome variation after 50 generations of radiation exposure in a wild rodent
Currently, the effects of chronic, continuous low dose environmental irradiation on the mitochondrial genome of resident small mammals are unknown. Using the bank vole (Myodes glareolus) as a model system, we tested the hypothesis that approximately 50 generations of exposure to the Chernobyl environment has significantly altered genetic diversity of the mitochondrial genome. Using deep sequencing, we compared mitochondrial genomes from 131 individuals from reference sites with radioactive contamination comparable to that present in Northern Ukraine before the April 26, 1986 meltdown, to populations where substantial fallout was deposited following the nuclear accident. Population genetic variables revealed significant differences among populations from contaminated and uncontaminated localities. Therefore, we rejected the null hypothesis of no significant genetic effect from 50 generations of exposure to the environment created by the Chernobyl meltdown. Samples from contaminated localities exhibited significantly higher numbers of haplotypes and polymorphic loci, elevated genetic diversity, and a significantly higher average number of substitutions-per-site across mitochondrial gene regions. Observed genetic variation was dominated by synonymous mutations, which may indicate a history of purify selection against nonsynonymous or insertion/deletion mutations. These significant differences were not attributable to sample size artifacts. The observed increase in mitochondrial genomic diversity in voles from radioactive sites is consistent with the possibility that chronic, continuous irradiation resulting from the Chernobyl disaster has produced an accelerated mutation rate in this species over the last 25 years. Our results, being the first to demonstrate this phenomenon in a wild mammalian species, are important for understanding genetic consequences of exposure to low-dose radiation sources.
Data from: Chronic exposure to neonicotinoids reduces honey bee health near corn crops
Experiments linking neonicotinoids and declining bee health have been criticized for not simulating realistic exposure. Here we quantified the duration and magnitude of neonicotinoid exposure in Canada's corn-growing regions and used these data to design realistic experiments to investigate the effect of such insecticides on honey bees. Colonies near corn were naturally exposed to neonicotinoids for up to 4 months—the majority of the honey bee's active season. Realistic experiments showed that neonicotinoids increased worker mortality and were associated with declines in social immunity and increased queenlessness over time. We also discovered that the acute toxicity of neonicotinoids to honey bees doubles in the presence of a commonly encountered fungicide. Our work demonstrates that field-realistic exposure to neonicotinoids can reduce honey bee health in corn-growing regions.
Data from: Exposure to predators does not lead to the evolution of larger brains in experimental populations of threespine stickleback
Natural selection is often invoked to explain differences in brain size among vertebrates. However, the particular agents of selection that shape brain size variation remain obscure. Recent studies suggest that predators may select for larger brains because increased cognitive and sensory abilities allow prey to better elude predators. Yet, there is little direct evidence that exposure to predators causes the evolution of larger brains in prey species. We experimentally tested this prediction by exposing families of 1000-2000 F2 hybrid benthic-limnetic threespine stickleback to predators under naturalistic conditions, along with matched controls. After two generations of selection, we found that fish from the predator addition treatment had significantly smaller brains (specifically smaller telencephalons and optic lobes) than fish from the control treatment. After an additional generation of selection, we reared experimental fish in a common environment and found that this difference in brain size was maintained in the offspring of fish from the predator addition treatment. Our results provide direct experimental evidence that (a) predators can indeed drive the evolution of brain size – but not in the fashion commonly expected and (b) that the tools of experimental evolution can be used to the study the evolution of the vertebrate brain.
Data from: Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmission
Prions that cause chronic wasting disease (CWD) in cervids can remain infective for years outside the host. Infectious cervids shed prions for a long time, consequently depositing prions in frequently used areas. These environmental prions are important in CWD epidemiology. Unfortunately, effective tools for quantifying CWD prions in soil, water, and other environmental sources are not currently available. Our goal was to investigate relative differences in visits by mule deer (Odocoileus hemionus hemionus) to various environmental site types as an indicator of the relative risk of prion contamination and disease transmission. For this, we deployed a system of triggered-by-movement cameras at eight site types in a CWD-endemic area in Saskatchewan, Canada. We first assessed whether the relative differences among site types in the frequency of visits by mule deer of any sex-and-age class, males, and females varied by season and site type. We then assessed whether the rate of behaviors with a high risk of environmental prion transmission (either contamination or acquisition) differed by season and site type. Finally, we assessed whether the intensity of visitation, based on the number of animals per picture, differed by season and site type. We found that grain sources and beds were key attractants for mule deer: (1) The greatest number of pictures with mule deer per camera-day occurred at grain sources across all seasons, except in fawning, when beds were the most visited sites; (2) during pre-rut and early gestation, mule deer visited grain sources at least twice as often as most other sites; (3) females were more likely to visit beds and grain sources, but there was no significant site preferences for males after accounting for season; (4) mule deer were most likely to be pictured contacting the environment at grain sources in early gestation; and (5) beds and grain sources were the most intensively visited sites. We also found that environmental contacts at waterholes were more frequent during spring. We discuss the potential importance of various sites in the transmission of CWD and how their modification could potentially reduce the risk of prion environmental exposure among mule deer.
Data from: Maladaptation to acute metal exposure in resurrected Daphnia ambigua clones after decades of increasing contamination
Human environmental impacts have driven some of the strongest and fastest phenotypic changes recorded in wild animal populations. Across populations, this variation is often adaptive, as populations evolve fitness advantages in response to human-modified environments. Yet some populations fail to adapt to changing environments. Evidenced by declines in relative fitness, such seemingly maladaptive outcomes are less common, but may be more likely in human modified contexts. Further, our ability to investigate the dynamics of these adaptive and maladaptive responses over time is typically limited in natural systems. I combined resurrection ecology and paleolimnology approaches to examine evolutionary responses of the freshwater zooplankter Daphnia to exposure to heavy metal contamination over the past 50-75 years using animals hatched from diapausing egg banks. In contrast to the predicted trend of adaptation to metal exposure over time, I observed an increase in sensitivity to both copper and cadmium exposure associated with increasing historic contamination. This potentially maladaptive trend occurred in Daphnia populations in three lakes. Given that the release of toxicants such as heavy metals is widespread and other researchers have observed local maladaptation to toxicant exposure, it is important to understand the drivers and implications of this pattern.
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.