Understanding the genetic architecture of quantitative traits can provide insights into the mechanisms driving phenotypic evolution. Bill morphology is an ecologically important and phenotypically variable trait, which is highly heritable and closely linked to individual fitness. Thus, bill morphology traits are suitable candidates for gene mapping analyses. Previous studies have revealed several genes that may influence bill morphology, but the similarity of gene and allele effects between species and populations is unknown. Here, we develop a custom 200K SNP array and use it to examine the genetic basis of bill morphology in 1857 house sparrow individuals from a large-scale, island metapopulation off the coast of Northern Norway. We found high genomic heritabilities for bill depth and length, which were comparable with previous pedigree estimates. Candidate gene and genomewide association analyses yielded six significant loci, four of which have previously been associated with craniofacial development. Three of these loci are involved in bone morphogenic protein (BMP) signalling, suggesting a role for BMP genes in regulating bill morphology. However, these loci individually explain a small amount of variance. In combination with results from genome partitioning analyses, this indicates that bill morphology is a polygenic trait. Any studies of eco-evolutionary processes in bill morphology are therefore dependent on methods that can accommodate polygenic inheritance of the phenotype and molecular-scale evolution of genetic architecture.

Telomeres are nucleoprotein structures that cap the ends of linear chromosomes in most eukaryotes (Blackburn, 1991). Understanding the causes of individual variation in telomere length (TL) is important because this trait has been shown to predict variation in survival or lifespan within and among species, particularly in birds (Bize

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Due to its history of multiple introductions to novel environments worldwide, the house sparrow has been used as a model species to study local adaption in invasive avian species. New genomic resources such as a custom 200K SNP array and a house sparrow reference genome provide great prospects for studying rapid local adaptation in this invasive species. Here, we analyse high-density genomewide genetic data collected across an extensive range of temperate, arid and tropical climates, in Australian populations that were introduced from Europe 150 years ago. We used two population differentiation (PD) and two ecological association (EA) methods to identify putative loci subject to selection across these varied climates. A majority of the outlier SNPs were identified through the use of the latent factor mixed models (LFMM) EA method, but the BayeScEnv EA method had the strongest overlap with the outliers from the two PD methods. Out of all the 971 outliers identified across the different methods, 38.3% were physically linked (within 20 kbps) to 575 known protein-coding regions in the house sparrow reference genome. Interestingly, some outlier genes had been previously identified in genome scan studies of broadly distributed species or had strong links to traits that are expected to be important to local adaptation, for example, heat-shock proteins, immune response and HOX genes. However, many outliers still have unknown relevance and some outliers can be false positives. Our results identify an opportunity to use the house sparrow model to further study local adaptation in an invasive species.

Metals and metalloids at elevated concentrations can be toxic to both humans and wildlife. In particular, lead exposure can act as a stressor to wildlife and cause negative effects on fitness. Any ability to adapt to stress caused by the negative effects of trace metal exposure would be beneficial for species living in contaminated environments. However, mechanisms for responding adaptively to metal contamination are not fully understood in free-living organisms. The Australian populations of the house sparrow (Passer domesticus) provides an excellent opportunity to study potential adaptation to environmental lead contamination because they have a commensal relationship with humans and are distributed broadly across Australian settlements including many long-term mining and smelting communities. To examine the potential for an evolutionary response to long-term lead exposure, we collected genomic SNP data using the house sparrow 200 K SNP array, from 11 localities across the Australian distribution including two mining sites (Broken Hill and Mount Isa, which are two genetically independent populations) that have well-established elevated levels of lead contamination as well as trace metals and metalloids. We contrast these known contaminated locations to other lesser-contaminated environments. Using an ecological association genome scan method to identify genomic differentiation associated with estimates of lead contamination we identified 60 outlier loci across three tests. A total of 39 genes were found to be physically linked (within 20 kbps) of all outliers in the house sparrow reference genome. The linked candidate genes included 12 genes relevant to lead exposure, such as two metal transporters that can transport metals including lead and zinc across cell membranes. These candidate genes provide targets for follow up experiments comparing resilience to lead exposure between populations exposed to varied levels of lead contamination.

Early-life telomere length (TL) is associated with fitness in a range of organisms. Little is known about the genetic basis of variation in TL in wild animal populations, but to understand the evolutionary and ecological significance of TL it is important to quantify the relative importance of genetic and environmental variation in TL. In this study, we measured TL in 2746 house sparrow nestlings sampled across 20 years and used an animal model to show that there is a small heritable component of early-life TL (h2=0.04), but with a strong component of maternal inheritance. Variation in TL among individuals was mainly driven by environmental (year) variance, but also brood and parental effects. We did not find evidence for a negative genetic correlation underlying the observed negative phenotypic correlation between TL and structural body size. Thus, TL may evolve independently of body size and the negative phenotypic correlation is likely to be caused by non-genetic environmental effects. We further used genome‐wide association analysis to identify genomic regions associated with TL variation. We identified several putative genes underlying TL variation; these have been inferred to be involved in oxidative stress, cellular growth, skeletal development, cell differentiation and tumorigenesis in other species. Together, our results show that TL is a lowly heritable, polygenic trait which is strongly affected by environmental conditions in a free-living bird.

Sexual dimorphism is often mediated by tissue-specific, differential gene expression, but the mechanisms that regulate these gene expression patterns are not well understood. Here, we investigate DNA methylation as a potential regulator of sex-biased gene expression in the house sparrow Passer domesticus. First, we examine whether sex-bias in gene expression or DNA methylation is present in this species, and whether any sex differences are tissue-general or tissue-specific. Second, we assess the correlation between gene expression and DNA methylation at different genomic features in several tissues. Samples clustered by tissue type when looking at both gene expression and DNA methylation, and in gonads samples clustered according to sex. We demonstrate sex-bias in DNA methylation and gene expression on the Z-chromosome as well as on autosomes, but find that most of the sex-biased genes are tissue-specific and that the majority of sex-bias occurs in gonads, although some tissue-general sex differences were observed. This underscores the importance of choosing a tissue relevant to the studied phenotype in DNA methylation or gene expression studies. We find strong negative correlation between DNA methylation and gene expression at the transcription start site (TSS), and that the TSS of highly expressed genes is hypomethylated in comparison to the TSS of genes with low expression. Furthermore, we show that sex-biased DNA methylation can account for 14% of the sex differences in gene expression in gonads. Together these results indicate that DNA methylation differences between the sexes can provide a mechanistic explanation for sex-biased gene expression that likely contributes to trait sexual dimorphism in nature.

Parasites can exert strong selective pressures on their hosts and influence the evolution of host immunity. While several studies have examined the genetic basis for parasite resistance, the role of epigenetics in the immune response to parasites is less understood. Yet, epigenetic modifications, such as changes in DNA methylation, may allow species to respond rapidly to parasite prevalence or virulence. To test the role of DNA methylation in relation to parasite infection, we examined genome‐wide DNA methylation before and during infection by a parasitic nematode, Syngamus trachea , in a natural population of house sparrows ( Passer domesticus ) using reduced representation bisulfite sequencing (RRBS). We found that DNA methylation levels were slightly lower in infected house sparrows, and we identified candidate genes relating to the initial immune response, activation of innate and adaptive immunity, and mucus membrane functional integrity that were differentially methylated between infected and control birds. Subsequently, we used methylation‐sensitive high‐resolution melting (MS‐HRM) analyses to verify the relationship between methylation proportion and S. trachea infection status at two candidate genes in a larger sample dataset. We found that methylation level at NR1D1 , but not CLDN22 , remained related to infection status and that juvenile recruitment probability was positively related to methylation level at NR1D1 . This underscores the importance of performing follow‐up studies on candidate genes. Our findings demonstrate that plasticity in the immune response to parasites can be epigenetically mediated and highlight the potential for epigenetic studies in natural populations to provide further mechanistic insight into host–parasite interactions.