Abstract
Pollutants, such as toxic metals, negatively influence organismal health and performance, even leading to population collapses. Studies in model organisms have shown that epigenetic marks, such as DNA methylation, can be modulated by various environmental factors, including pollutants, influencing gene expression, and various organismal traits. Yet experimental data on the effects of pollution on DNA methylation from wild animal populations are largely lacking. We here experimentally investigated for the first time the effects of early-life exposure to environmentally relevant levels of a key pollutant, arsenic (As), on genome-wide DNA methylation in a wild bird population. We experimentally exposed nestlings of great tits (Parus major) to arsenic during their postnatal developmental period (3 to 14 days post-hatching) and compared their erythrocyte DNA methylation levels to those of respective controls. In contrast to predictions, we found no overall hypomethylation in the arsenic group. We found evidence for loci to be differentially methylated between the treatment groups, but for five CpG sites only. Three of the sites were located in gene bodies of zinc finger and BTB domain containing 47 (ZBTB47), HIVEP zinc finger 3 (HIVEP3), and insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1). Further studies are needed to evaluate whether epigenetic dysregulation is a commonly observed phenomenon in polluted populations and what are the consequences for organism functioning and for population dynamics.
Highlights
Environmental pollution can negatively affect organisms at multiple levels of organization, from molecular and physiological levels to performance, and even lead to population collapses.[1−4]In wild populations, a largely unexplored mechanism mediating such pollution effects is the potential influence of the epigenome, such as DNA methylation
DNA methylation is the addition of a methyl (−CH3) group to the 5′ carbon site of cytosines catalyzed by DNA methyltransferases and is generally found to be negatively associated with gene expression.[12]
In the subsample of nests selected for representation bisulfite sequencing (RRBS), the values were 0.47 ± 0.37 ppm for control nests and 6.50 ± 5.10 ppm for arsenic treatment, respectively
Summary
Environmental pollution can negatively affect organisms at multiple levels of organization, from molecular and physiological levels to performance, and even lead to population collapses.[1−4]In wild populations, a largely unexplored mechanism mediating such pollution effects is the potential influence of the epigenome, such as DNA methylation. In human and animal models, the effects of pollution on the epigenome are studied extensively, and it has been discovered that methylation patterns can be changed by various environmental factors, including metal and organic pollutants and other early-life stressors (reviewed by refs 5−11). DNA methylation is the addition of a methyl (−CH3) group to the 5′ carbon site of cytosines catalyzed by DNA methyltransferases and is generally found to be negatively associated with gene expression.[12] Variation in DNA methylation is linked to variation in phenotypes and behavior, and associated with the prevalence of various diseases, including cancers in humans and model animals.[13−16] Epigenetic changes from early-life environment may persist and affect health throughout lifetime and may even be transmitted to future generations,[16] which could potentially contribute to explaining delayed or persistent effects of pollutants (e.g., ref 7). Arsenic can have negative consequences for basically all organ systems, often via causing oxidative stress, i.e., the imbalance between harmful reactive oxygen species (ROS) and antioxidant defenses, and cancer.[27,28]
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