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.

越来越多的研究证据表明，在各类群生物中，处于繁殖竞争环境的雌性个体往往会在产前向后代分配更多睾酮，其后代通常表现出更具攻击性、生长速度更快的表型。截至目前，尚无研究阐明该母性效应影响后代表型的具体介导机制。不过，雌激素受体α（estrogen receptor alpha, ERα）的基因表达水平与个体早期生长和攻击性差异存在关联；据此推测，母体激素或许可在后代产前发育阶段，通过DNA甲基化等途径调控ERα基因的表达。我们开展了一项预实验，旨在探究不同繁殖密度下野生东蓝鸲（Sialia sialis）通过卵黄向后代分配睾酮的自然变异，以及后代生长与行为相关脑区中ERα启动子区域CG二核苷酸的DNA甲基化水平。我们提出如下研究假说：繁殖密度与卵黄睾酮浓度呈正相关；产前暴露于母体来源的卵黄睾酮，会与后代更快的生长速率以及更低的ERα启动子甲基化水平相关联。实验结果显示，卵黄睾酮浓度与繁殖密度、雏鸟生长速率，以及间脑ERα启动子5个待检测CpG位点中的位点3的DNA甲基化百分比呈正相关，但端脑未检测到此类关联（样本量n=10）。间脑CpG位点3的DNA甲基化百分比与雏鸟生长速率呈正相关。上述数据表明，表观遗传可能在介导母性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，将有助于阐明动物响应环境的关键途径。此外，通过阐明母性效应的介导机制，我们能够进一步理解这些机制的遗传潜力，以及母性效应在进化尺度上所能产生的综合影响。