Data from: Relationship between maternal environment and DNA methylation patterns of estrogen receptor alpha in wild Eastern Bluebird (Sialia sialis) nestlings: a pilot study

There is mounting evidence that, across taxa, females breeding in competitive environments tend to allocate more testosterone to their offspring prenatally and these offspring typically have more aggressive and faster-growing phenotypes. To date, no study has determined the mechanisms mediating this maternal effect's influence on offspring phenotype. However, levels of estrogen receptor alpha (ERα) gene expression are linked to differences in early growth and aggression; thus, maternal hormones may alter gene regulation, perhaps via DNA methylation, of ERα in offspring during prenatal development. We performed a pilot study to examine natural variation in testosterone allocation to offspring through egg yolks in wild Eastern Bluebirds (Sialia sialis) in varying breeding densities and percent DNA methylation of CG dinucleotides in the ERα promoter in offspring brain regions associated with growth and behavior. We hypothesized that breeding density would be positively correlated with yolk testosterone, and prenatal exposure to maternal-derived yolk testosterone would be associated with greater offspring growth and decreased ERα promoter methylation. Yolk testosterone concentration was positively correlated with breeding density, nestling growth rate, and percent DNA methylation of one out of five investigated CpG sites (site 3) in the diencephalon ERα promoter, but none in the telencephalon (n = 10). Percent DNA methylation of diencephalon CpG site 3 was positively correlated with growth rate. These data suggest a possible role for epigenetics in mediating the effects of the maternal environment on offspring phenotype. Experimentally examining this mechanism with a larger sample size in future studies may help elucidate a prominent way in which animals respond to their environment. Further, by determining the mechanisms that mediate maternal effects, we can begin to understand the potential for the heritability of these mechanisms and the impact that maternal effects are capable of producing at an evolutionary scale.

越来越多的证据表明，在不同分类群（taxa）中，处于竞争繁殖环境的雌性往往会在产前向后代分配更多睾酮（testosterone），而这些后代通常会表现出更具攻击性、生长速度更快的表型（phenotypes）。迄今为止，尚无研究阐明这种母体效应（maternal effect）影响后代表型的介导机制。不过，雌激素受体α（ERα，estrogen receptor alpha）的基因表达水平与早期生长和攻击性差异相关；因此，母体激素可能在产前发育过程中，通过DNA甲基化（DNA methylation）等途径改变后代体内ERα的基因调控。本研究开展了一项预实验（pilot study），旨在探究不同繁殖密度（breeding densities）下野生东蓝鸲（Sialia sialis）通过卵黄（egg yolks）向后代分配睾酮的自然变异情况，以及后代体内与生长和行为相关脑区中ERα启动子（promoter）区域CG二核苷酸（CG dinucleotides）的DNA甲基化水平。我们提出如下假说：繁殖密度与卵黄睾酮浓度呈正相关，且产前暴露于母体来源的卵黄睾酮与后代更快的生长速率以及ERα启动子甲基化水平降低相关。研究结果显示，卵黄睾酮浓度与繁殖密度、雏鸟生长速率，以及间脑（diencephalon）ERα启动子区域5个检测CpG位点（CpG sites）中的位点3的DNA甲基化水平呈正相关，但端脑（telencephalon）区域未发现此类关联（样本量n=10）。间脑CpG位点3的DNA甲基化水平与雏鸟生长速率呈正相关。上述结果表明，表观遗传学（epigenetics）可能在介导母体环境对后代表型的影响中发挥潜在作用。未来通过更大样本量开展实验验证该机制的研究，或有助于阐明动物响应环境的重要途径。此外，通过阐明介导母体效应的机制，我们能够进一步理解这些机制的遗传潜力（heritability），以及母体效应在进化尺度（evolutionary scale）上所能产生的影响。