| dc.description.abstract | Parasites are important drivers of ecological and evolutionary processes in natural populations, and can exert strong selective pressures on their hosts by reducing host fitness. Investigating the mechanisms involved in defence against parasites is therefore important to understand how populations are likely to respond to changes in parasite prevalence or virulence. I used data from a house sparrow-nematode study system to show that inherited genetic differences, DNA methylation changes, development of acquired immunity, and extrinsic factors together contribute to defence against parasites in natural populations.
I demonstrate that resistance against the parasitic nematode, Syngamus trachea, is polygenic in house sparrows (Passer domesticus), that there exists substantial additive and dominance genetic variance in resistance, and identified several candidate genes for parasite resistance (Paper I). Thus, standing genetic variation may allow natural populations to respond to changes in parasite pressure.
I found that gene expression was strongly negatively correlated with DNA methylation at the transcription start site (TSS) of genes in the house sparrow, regardless of tissue of origin, and found extensive sex-bias in gene expression and DNA methylation that was tissue-specific in nature (Paper II). This tissue-specificity highlights the importance of choosing a tissue relevant to the studied phenotype in DNA methylation studies. Furthermore, I present evidence of an epigenetic signature of parasitism of house sparrows by S. trachea (Paper III). Thus, DNA methylation may play an additional role to genetic variation in defence against parasites by allowing organisms to mount a plastic response to immune challenge.
Next, I quantified antibody-mediated immunity in house sparrows living in pathogen-rich vs low pathogen environments, and investigated whether S. trachea antigen-specific IgY levels were higher in parasitised individuals (Paper IV). I found that antibody-mediated immunity may differ between environments and age classes, and that the ability to mount an appropriate antibody response to parasites may contribute to differences in survival probability.
Finally, I provide empirical evidence that both population density and S. trachea parasite load negatively impact house sparrow survival probability, and demonstrate that the density-dependent relationship between survival probability and parasite load differed in strength between adults and juveniles (Paper V). Furthermore, juvenile survival probability was negatively related to genetic susceptibility to this parasite. Accordingly, the effects of population density and parasite load on fitness may be closely linked and modulated by genetic differences in individual risk, and the strength of any ecological feedback caused by the density-dependent effects of parasite load on fitness may depend on the age structure of population
In summary, these results demonstrate that both inherited resistance genotypes and DNA methylation differences between individuals may be important in defence against parasites, that differences in immunocompetence may explain the differing survival rates of adults and juveniles infected by parasites, and that there can exist density-dependent effects of parasite load on fitness that may have the potential to cause ecological feedback by influencing population growth rates. As such, this work extends current understanding of the mechanisms underlying defence against parasites and of how parasites may impact both individual fitness and population demography. | en_US |
