For over 50 years, the great tit (Parus major) has been a model species for research in evolutionary, ecological and behavioural research; in particular, learning and cognition have been intensively studied. Here, to provide further insight into the molecular mechanisms behind these important traits, we de novo assemble a great tit reference genome and whole-genome re-sequence another 29 individuals from across Europe. We show an overrepresentation of genes related to neuronal functions, learning and cognition in regions under positive selection, as well as increased CpG methylation in these regions. In addition, great tit neuronal non-CpG methylation patterns are very similar to those observed in mammals, suggesting a universal role in neuronal epigenetic regulation which can affect learning-, memory- and experience-induced plasticity. The high-quality great tit genome assembly will play an instrumental role in furthering the integration of ecological, evolutionary, behavioural and genomic approaches in this model species.
Summary 1.Parasites can affect host fitness, provoke host responses, and thereby mediate host life history evolution. As life history strategies are often sex-specific, immunological or behavioural responses of the host aiming to reduce the impact of parasites may be sexually dimorphic, e.g. as a consequence of sex differences in the resource allocation tradeoff between parasite defence, morphological traits and body functions. Parasites may therefore affect males and females differently leading to sex specific patterns of parasite susceptibility. 2.In an experimental field study, we manipulated the ectoparasite load of great tit nests ( Parus major ) and investigated its effects on male and female nestlings. As susceptibility to parasites may be linked to the ability of the nestlings to fight off parasites immunologically, we further investigated sex differences in cell-mediated immunity using a phytohaemagglutinin (PHA) assay. 3. Body mass, metatarsus length and overall body size, but not feather length, showed a sexual dimorphism at the end of the nestling period. A significant interaction between the effects of sex and parasite treatment on the sexually dimorphic traits indicates that the parasite effect is sex-specific. While no differences in morphological traits were found in females raised in infested and uninfested nests, parasitized males were significantly smaller and lighter than males raised in uninfested nests. Further, we found a pronounced sexual dimorphism in the response to the PHA assay with males showing a reduced cellular immunity. The parasite treatment had a non-significant effect on the PHA response and the PHA response of males and females were not influenced differently by parasites. 4. Our study shows that sexual dimorphism in susceptibility to parasites and immunocompetence develops early in life, and suggests sex-specific strategies in the allocation of limited resources. Possible mechanisms of sex differences in susceptibility to parasites and immunocompetence during postnatal growth and the consequences for optimal sex allocation strategies of the parents are discussed.
Many vertebrates use carotenoid-based signals in social or sexual interactions. Honest signalling via carotenoids implies some limitation of carotenoid-based colour expression among phenotypes in the wild, and at least five limiting proximate mechanisms have been hypothesized. Limitation may arise by carotenoid-availability, genetic constraints, body condition, parasites, or detrimental effects of carotenoids. An understanding of the relative importance of the five mechanisms is relevant in the context of natural and sexual selection acting on signal evolution. In an experimental field study with carotenoid supplementation, simultaneous cross-fostering, manipulation of brood size and ectoparasite load, we investigated the relative importance of these mechanisms for the variation in carotenoid-based coloration of nestling great tits (Parus major). Carotenoid-based plumage coloration was significantly related to genetic origin of nestlings, and was enhanced both in carotenoid-supplemented nestlings, and nestlings raised in reduced broods. We found a tendency for ectoparasite-induced limitation of colour expression and no evidence for detrimental effects of carotenoids on growth pattern, mortality and recruitment of nestlings to the local breeding population. Thus, three of the five proposed mechanisms can generate individual variation in the expression of carotenoid-based plumage coloration in the wild and thus could maintain honesty in a trait potentially used for signalling of individual quality.
The discovery of the key role of Toll-like receptors (TLRs) in initiating innate immune responses and modulating adaptive immunity has revolutionized our understanding of vertebrate defence against pathogens. Yet, despite their central role in pathogen recognition and defence initiation, there is little information on how variation in TLRs influences disease susceptibility in natural populations. Here, we assessed the extent of naturally occurring polymorphisms at TLR2 in wild bank voles (Myodes glareolus) and tested for associations between TLR2 variants and infection with Borrelia afzelii, a common tick-transmitted pathogen in rodents and one of the causative agents of human Lyme disease. Bank voles in our population had 15 different TLR2 haplotypes (10 different haplotypes at the amino acid level), which grouped in three well-separated clusters. In a large-scale capture-markrecapture study, we show that voles carrying TLR2 haplotypes of one particular cluster (TLR2 c2 ) were almost three times less likely to be Borrelia infected than animals carrying other haplotypes. Moreover, neutrality tests suggested that TLR2 has been under positive selection. This is, to our knowledge, the first demonstration of an association between TLR polymorphism and parasitism in wildlife, and a striking example that genetic variation at innate immune receptors can have a large impact on host resistance.
Maternal effects can adaptively modulate offspring developmental trajectories in variable but predictable environments. Hormone synthesis is sensitive to environmental factors, and maternal hormones are thus a powerful mechanism to transfer environmental cues to the next generation. Birds have become a key model for the study of hormone-mediated maternal effects because the embryo develops outside the mother's body, facilitating the measurement and manipulation of prenatal hormone exposure. At the same time, birds are excellent models for the integration of both proximate and ultimate approaches, which is key to a better understanding of the evolution of hormone-mediated maternal effects. Over the past two decades, a surge of studies on hormone-mediated maternal effects has revealed an increasing number of discrepancies. In this review, we discuss the role of the environment, genetic factors and social interactions in causing these discrepancies and provide a framework to resolve them. We also explore the largely neglected role of the embryo in modulating the maternal signal, as well as costs and benefits of hormone transfer and expression for the different family members. We conclude by highlighting fruitful avenues for future research that have opened up thanks to new theoretical insights and technical advances in the field. This article is part of the theme issue ‘Developing differences: early-life effects and evolutionary medicine’.
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