Impacts of urbanisation on birds : Disentangling the effects of multiple pollutants on avian behaviour and physiology

Anthropogenic pollution is a pervasive feature of urbanisation, reaching into ecosystems worldwide and posing novel challenges to wildlife. Not surprisingly, differences in behaviour, and physiology, have been found between urban and rural populations. Most studies on anthropogenic impacts have so far either used a dichotomous approach, comparing urban-rural sites, or investigated impacts of just one stressor. However, urban environments create a complex matrix of co-occuring pollutants, leading to potentially complex interactive effects between stressors. We currently lack a deeper knowledge of the combined and single effects and the underlying mechanisms creating urban-rural phenotypic variation. In this thesis, I investigated the single and combined effects of urban pollutants of avian behaviour and physiology. Specifically, I used the oxidative stress system, immune system, and plasma fatty acid composition, as the key physiological traits responding to human-induced environmental change. Urban pollutants of interest were artificial light at night (ALAN), anthropogenic noise, ozone and soot, and as human-influenced additional factors I looked at impacts of differential diets, and vegetation structure. I utilised full-factorial experimental exposure experiments in the wild and in the laboratory, and a correlative study in the wild, using wild and captive birds.I found that ALAN exposure alone decreases activity and noise exposure alone decreases the proportion of birds found feeding. The combined exposure to these two pollutants led to a non-additive effect on the proportion of birds resting, with ALAN as the driving stressor. ALAN-exposed nestlings mounted a less strong immune response, with a reduction of melatonin levels being the likely mechanistic link to an impaired immune functioning. Simultaneous exposure to ALAN and noise increased levels of an important antioxidant, total glutathione, more than the additive effect from single pollutant effects would have estimated (positive synergistic effect). Furthermore, I found that ozone is a potent pro-oxidant, negatively affecting antioxidant capacity, but we found no increased levels of oxidative damage due to ozone exposure. Soot exposure, on the other hand, did not affect avian oxidative stress status. Dietary ω6- and ω3-polyunsaturated fatty acids (PUFAs) modulated oxidative stress response to ozone exposure, but also act alone, with ω3-PUFAs decreasing non-enzymatic antioxidant capacity. Likewise, ω6:ω3 ratios of circulating PUFAs of wild nestlings are changed by human-influenced environmental factors, as well as their antioxidant capacity is negatively affected by air pollution and number of oak trees around their nest box. We also showed in this latter study, that using multi-stressor approach gives a more profound mechanistic understanding of phenotypic effects, then using a dichotomous comparison, which might obscure certain effects. Overall, I show that pollutants affect behaviour and key fitness related physiological traits and that the combined exposure to multiple stressors can lead to unexpected non-additive effects. This highlights the need of a more thorough mechanistic understanding of multi-stressor effects. A deeper understanding of single and combinatory effects of anthropogenic stressors will help gaining crucial insight into populations and species resilience to environmental change, thereby targeted actions can be proposed to maintain biodiversity in cities and have a future development of sustainable cities

Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation

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

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

Sustainable product development by means of personalization – paradox or solution?

Personalization of products and services entails not only risks but also potentials for sustainability. During the product development process, it is crucial to take into account future usage patterns and their variability. Even if the product itself is not personalized, a user-centered approach during the entire life cycle can unlock many potentials. Avoiding unnecessary functions and tailoring a product precisely to its user’s needs can lead to optimized sustainability performance during its use. Moreover, by developing and offering personalizable products that meet the requirements of the respective user, companies can tap into new market opportunities and increase their competitiveness. As a methodological basis, we introduce a combination of the Stuttgart models of personalization and personalized product development with life cycle thinking aspects and circularity strategies. In an interactive workshop the integrated model is discussed and participants can locate their own work and perspective within the broader personalization scheme. Different opportunities of personalization are highlighted from an environmental point of view

Interactive effects of yolk testosterone and carotenoid on prenatal growth and offspring physiology in a precocial bird

Conditions experienced by individuals during prenatal development can have long-term effects on their phenotype. Maternally transmitted resources are important mediators of such prenatal effects, but the potential interactive effects among them in shaping offspring phenotype have never been studied. Maternally derived testosterone is known to stimulate growth, but these benefits may be counterbalanced by an increase in the production of reactive oxygen species (ROS). Maternally transmitted carotenoids might have the capacity to scavenge ROS and thereby buffer an increase in oxidative stress caused by prenatal exposure to high testosterone levels. Here, we experimentally tested for such interactive effects between maternal yolk testosterone and carotenoid in Japanese quail (Coturnix japonica). We found that hatching mass was reduced and reactive oxygen metabolites (ROMs) levels at the end of the period of maximal growth increased in chicks from eggs injected with either testosterone or carotenoid (only a tendency in chicks from testosterone-injected eggs). However, when both egg compounds were manipulated simultaneously, hatching mass and ROM levels were not affected, showing that both carotenoid and testosterone lose their detrimental effects when the ratio between the 2 compounds is balanced. Our study provides the first experimental evidence for interactive effects of 2 maternally derived egg compounds on offspring phenotype and suggests that developmental cues are tightly coadjusted within an egg

Data Biol.Lett_testes size

Dat

Data from: Matrilineal inheritance of a key mediator of prenatal maternal effects

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

Data from: Matrilineal inheritance of a key mediator of prenatal maternal effects

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

High Yolk Testosterone Transfer Is Associated with an Increased Female Metabolic Rate

Yolk androgens of maternal origin are important mediators of prenatal maternal effects. Although in many species short-term benefits of exposure to high yolk androgen concentrations for the offspring have been observed, females differ substantially in the amount of androgens they transfer to their eggs. It suggests that costs for the offspring or the mother constrain the evolution of maternal hormone transfer. However, to date, the nature of these costs remains poorly understood. Unlike most previous work that focused on potential costs for the offspring, we here investigated whether high yolk testosterone transfer is associated with metabolic costs (i.e., a higher metabolic rate) for the mother. We show that Japanese quail (Coturnix japonica) females that deposit higher testosterone concentrations into their eggs have a higher resting metabolic rate. Because a higher metabolic rate is often associated with a shorter life span, this relationship may explain the negative association between yolk testosterone transfer and female longevity observed in the wild. Our results suggest that metabolic costs for the mother can balance the short-term benefits of yolk testosterone exposure for the offspring, thereby contributing to the maintenance of variation in maternal yolk hormone transfer in natural populations