Interactive and Long-term Effects of Yolk Androgens and Antioxidants in Birds

This is the author accepted manuscript. The final version is available from OUP via the DOI in this recordPoster abstract - Annual Meeting of the Society-for-Integrative-and-Comparative-Biology (SICB), 4-8 January 2017, New Orleans, US

Do telomeres influence pace-of-life-strategies in response to environmental conditions over a lifetime and between generations?

This is the author accepted manuscript. The final version is available from Wiley via the DOI in this recordEuropean Union Horizon 2020Estonian Research Counci

Long-term effect of yolk carotenoid levels on testis size in a precocial bird

This is the author accepted manuscript. The final version is available from the Royal Society via the DOI in this record.Conditions experienced during prenatal development can have long-lasting organizational effects on offspring. Maternal carotenoids deposited in the eggs of birds and other oviparous species play an important role during fast embryonic growth and chick development through their antioxidant properties. However, the long-term consequences of variation in maternal carotenoid transfer for the offspring have seldom been considered. Since plasma carotenoid levels at adulthood are known to influence testis size and yolk carotenoid levels influence the ability to extract carotenoids later in life, we hypothesized that maternally transmitted carotenoids might influence gonad size at adulthood. Here, we showed that male Japanese quail (Coturnix japonica) originating from a carotenoid-enriched egg had smaller testes than control individuals at adulthood. This result shows that yolk carotenoids have long-term organizational effects. In addition, given that carotenoid intake at sexual maturity increases sperm quality and that a decreased testis size is associated with a lower sperm production, we propose that carotenoid exposure during embryo development might influence a trade-off between ejaculate size and sperm quality.The study was supported by the Swiss National Science Foundation (PP00P3_128386 and PP00P3_157455) and the Fonds zur Förderung des akademischen Nachwuchses

In ovo yolk carotenoid and testosterone levels interactively influence female transfer of yolk antioxidants to her eggs

This is the author accepted manuscript. The final version is available from the Royal Society via the DOI in this recordMothers can influence prenatal conditions by varying the amount of nutrients, hormones or antioxidants they provide to their developing young. Some of these substances even affect the transfer of these compounds in the next generation, but it is less clear how different maternally transmitted compounds interact with each other to shape reproductive resource allocation in their offspring. Here, we found that female Japanese quail that were exposed to high carotenoid levels during embryonic development transferred lower concentrations of yolk antioxidants to their own eggs later in life. This effect disappeared, when both testosterone and carotenoid concentrations were manipulated simultaneously, showing long-term and interactive effects of these maternally derived egg components on a female’s own egg composition. Given that exposure to high levels of testosterone during embryo development stimulates the production of reactive oxygen (ROS) and impairs antioxidant defenses, we propose that carotenoids act as in-ovo antioxidants in an oxidatively stressful environment (i.e. when levels of testosterone are high) but might have prooxidant properties in an environment where they are not used to counteract an increased production of ROS. In line with this hypothesis, we previously showed that prenatal exposure to increased concentrations of yolk carotenoids leads to a rise of oxidative damage at adulthood, but only when yolk testosterone concentrations were not experimentally increased as well. As a consequence, antioxidants in the body may be used to limit oxidative damage in females exposed to high levels of carotenoids during development (but not in females exposed to increased levels of both carotenoids and testosterone), resulting in lower amounts of antioxidants being available for deposition into eggs. Since prenatal antioxidant exposure is known to influence fitness-related traits, the effect detected in this study might have transgenerational consequences.The study was supported by the Swiss National Science Foundation (PP00P3_128386 and PP00P3_157455) and the Fonds zur Förderung des akademischen Nachwuchses

Contrasting evolution of virulence and replication rate in an emerging bacterial pathogen

This is the final version. Available on open access from the National Academy of Sciences via the DOI in this recordData deposition: Data reported in this paper have been deposited in Dryad Digital Repository (doi:10.5061/dryad.km3109k).Host resistance through immune clearance is predicted to favor pathogens that are able to transmit faster and are hence more virulent. Increasing pathogen virulence is, in turn, typically assumed to be mediated by increasing replication rates. However, experiments designed to test how pathogen virulence and replication rates evolve in response to increasing host resistance, as well as the relationship between the two, are rare and lacking for naturally evolving host–pathogen interactions. We inoculated 55 isolates of Mycoplasma gallisepticum, collected over 20 y from outbreak, into house finches (Haemorhous mexicanus) from disease-unexposed populations, which have not evolved protective immunity to M. gallisepticum. We show using 3 different metrics of virulence (body mass loss, symptom severity, and putative mortality rate) that virulence has increased linearly over >150,000 bacterial generations since outbreak (1994 to 2015). By contrast, while replication rates increased from outbreak to the initial spread of resistance (1994 to 2004), no further increases have occurred subsequently (2007 to 2015). Finally, as a consequence, we found that any potential mediating effect of replication rate on virulence evolution was restricted to the period when host resistance was initially increasing in the population. Taken together, our results show that pathogen virulence and replication rates can evolve independently, particularly after the initial spread of host resistance. We hypothesize that the evolution of pathogen virulence can be driven primarily by processes such as immune manipulation after resistance spreads in host populations.Natural Environment Research Council (NERC

Matrilineal inheritance of a key mediator of prenatal maternal effects

This is the author accepted manuscript. The final version is available from the Royal Society via the DOI in this record.Sex-linkage is predicted to evolve in response to sex-specific or sexually antagonistic selection. In line with this prediction, most sex-linked genes are associated with reproduction in the respective sex. In addition to traits directly involved in fertility and fecundity, mediators of maternal effects may be predisposed to evolve sex-linkage, because they indirectly affect female fitness through their effect on offspring phenotype. Here, we test for sex-linked inheritance of a key mediator of prenatal maternal effects in oviparous species, the transfer of maternally derived testosterone to the eggs. Consistent with maternal inheritance, we found that in Japanese quail (Coturnix japonica) granddaughters resemble their maternal (but not their paternal) grandmother in yolk testosterone deposition. This pattern of resemblance was not due to non-genetic priming effects of testosterone exposure during prenatal development, as an experimental manipulation of yolk testosterone levels did not affect the females' testosterone transfer to their own eggs later in life. Instead, W chromosome and/or mitochondrial variation may underlie the observed matrilineal inheritance pattern. Ultimately, the inheritance of mediators of maternal effects along the maternal line will allow for a fast and direct response to female-specific selection, thereby affecting the dynamics of evolutionary processes mediated by maternal effects.The study was financially supported by Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (PP00P3_128386 and PP00P3_157455) and Fonds zur Förderung des akademischen Nachwuchses (FAN)

Rapid antagonistic coevolution in an emerging pathogen and its vertebrate host

This is the final version of the article. Available from Elsevier via the DOI in this record.Host-pathogen coevolution is assumed to play a key role in eco-evolutionary processes, including epidemiological dynamics and the evolution of sexual reproduction [1-4]. Despite this, direct evidence for host-pathogen coevolution is exceptional [5-7], particularly in vertebrate hosts. Indeed, although vertebrate hosts have been shown to evolve in response to pathogens or vice versa [8-12], there is little evidence for the necessary reciprocal changes in the success of both antagonists over time [13]. Here, we generate a time-shift experiment to demonstrate adaptive, reciprocal changes in North American house finches (Haemorhous mexicanus) and their bacterial pathogen, Mycoplasma gallisepticum [14-16]. Our experimental design is made possible by the existence of disease-exposed and unexposed finch populations, which were known to exhibit equivalent responses to experimental inoculation until the recent spread of genetic resistance in the former [14, 17]. While inoculation with pathogen isolates from epidemic outbreak caused comparable sub-lethal eye-swelling in hosts from exposed (hereafter adapted) and unexposed (hereafter ancestral) populations, inoculation with isolates sampled after the spread of resistance were threefold more likely to cause lethal symptoms in hosts from ancestral populations. Similarly, the probability that pathogens successfully established an infection in the primary host and, before inducing death, transmitted to an uninfected sentinel was highest when recent isolates were inoculated in hosts from ancestral populations and lowest when early isolates were inoculated in hosts from adapted populations. Our results demonstrate antagonistic host-pathogen coevolution, with hosts and pathogens displaying increased resistance and virulence in response to each other over time.This research was supported by a Natural Environment Research Council standard grant to C.B. (NE/M00256X)

Characterization of Susceptibility Artifacts in MR-thermometry PRFS-based during Laser Interstitial Thermal Therapy

Magnetic Resonance Thermometry (MRT) is demonstrating huge abilities to guide laser interstitial thermal therapy (LITT) in several organs, such as the brain. Among the methods to perform MRT, Proton Resonance Frequency (PRF) shift holds significant benefits, like tissue independence. Despite its potential, PRF shift-based MRT holds significant challenges affecting the accuracy of reconstructed temperature maps. In particular, susceptibility artifacts due to gas-bubble formation are an important source of error in temperature maps in MRT-guided LITT. This work presents the characterization of the susceptibility artifacts in MRT-guided LITT and the measurement of its size. LITT was performed in gelatin-based phantoms, at 5 W, 2 W, 1 W, and 0.5 W under MRI guidance with a 1.5 T clinical MRI scanner. Temperature images were obtained with a 3D EPI (Echo planar imaging) prototype sequence. Areas of temperature errors were defined as zones of negative temperature variation <-2 degrees C. Moreover, we have analyzed the artifact shape in sagittal, axial and coronal planes. The analysis demonstrates a double-lobe shape for the susceptibility artifact mainly distributed in the sagittal plane. Also, the higher laser power caused a bigger artifact area. Temperature errors of similar to 80 degrees C proved the necessity to avoid susceptibility artifact generation during MRT-guided LITT. The analysis of the influence of the laser power on the artifact has suggested that using low laser power (0.5 W) helps avoid this measurement error

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

Evolutionary Applications published by John Wiley & Sons Ltd Ecological and evolutionary concepts have been widely adopted to understand host–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–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–domestic–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

Experimental evidence for stabilizing selection on virulence in a bacterial pathogen

This is the final version. Available on open access from Wiley via the DOI in this recordData archiving: Data reported in this paper have been deposited in Dryad Digital Repository (https://doi.org/10.5061/dryad.9cnp5hqgh).The virulence‐transmission trade‐off hypothesis has provided a dominant theoretical basis for predicting pathogen virulence evolution, but empirical tests are rare, particularly at pathogen emergence. The central prediction of this hypothesis is that pathogen fitness is maximized at intermediate virulence due to a trade‐off between infection duration and transmission rate. However, obtaining sufficient numbers of pathogen isolates of contrasting virulence to test the shape of relationships between key pathogen traits, and doing so without the confounds of evolved host protective immunity (as expected at emergence), is challenging. Here, we inoculated 55 isolates of the bacterial pathogen, Mycoplasma gallisepticum, into non‐resistant house finches (Haemorhous mexicanus) from populations that have never been exposed to the disease. Isolates were collected over a 20‐year period from outbreak in disease‐exposed populations of house finches and vary markedly in virulence. We found a positive linear relationship between pathogen virulence and transmission rate to an uninfected sentinel, supporting the core assumption of the trade‐off hypothesis. Further, in support of the key prediction, there was no evidence for directional selection on a quantitative proxy of pathogen virulence and, instead, isolates of intermediate virulence were fittest. Surprisingly, however, the positive relationship between virulence and transmission rate was not underpinned by variation in pathogen load or replication rate as is commonly assumed. Our results indicate that selection favors pathogens of intermediate virulence at disease emergence in a novel host species, even when virulence and transmission are not linked to pathogen load.Natural Environment Research Council (NERC