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Data from: Exposure to a competitive social environment activates an epigenetic mechanism that limits pheomelanin synthesis in zebra finches

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Mendeley Data2024-06-25 更新2024-06-29 收录
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https://zenodo.org/records/5015577
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Competitive environments promote high testosterone levels, oxidative stress and, consequently, impair cellular homeostasis. The regulation of genes involved in the synthesis of the pigment pheomelanin in melanocytes seems to help to maintain homeostasis against environmental oxidative stress. Here, we experimentally increased social interactions in some zebra finch Taeniopygia guttata males by keeping them in groups of six birds during feather growth, while others were kept alone, to test if melanocytes show epigenetic lability under a competitive social environment. As these changes may depend on the oxidative status, we administrated buthionine sulfoximine (BSO) to decrease the antioxidant capacity of some birds. The competitive environment downregulated a gene involved in pheomelanin synthesis (Slc7a11) by changing the level of DNA methylation in feather melanocytes. In other genes involved in pheomelanin synthesis (Slc45a2, MC1R and AGRP), DNA methylation was also affected, but no changes in expression were detected. The exposure to the competitive environment did not affect systemic oxidative stress and damage, indicating that a protective epigenetic mechanism that changes the expression of Slc7a11 may have been activated. However, no changes on the pigmentation phenotype of birds were found, likely due to the short duration or low intensity of the competitive environment. BSO treatment did not affect the epigenetic mechanism, suggesting that the antioxidant capacity of birds was high enough to deal with the competitive environment. An epigenetic mechanism limiting pheomelanin synthesis gets therefore activated under exposure to a competitive environment in male zebra finches, which may help avoiding damage caused by competitive interactions.

竞争性环境可提升睾酮水平与氧化应激水平,进而损害细胞稳态。黑素细胞(melanocytes)中参与褐黑素(pheomelanin)合成的基因调控通路,似乎可助力机体抵御环境氧化应激以维持细胞稳态。本研究通过将部分雄性斑胸草雀(Taeniopygia guttata)在羽毛生长期饲养于6只个体的群体中,以增强其社会互动强度,其余个体则单独饲养,以此检验黑素细胞在竞争性社会环境下是否存在表观遗传不稳定性。鉴于此类表观遗传变化可能依赖于机体氧化状态,我们对部分受试个体施用了丁胱亚磺酰亚胺(buthionine sulfoximine, BSO)以降低其抗氧化能力。结果显示,竞争性环境可通过改变羽毛黑素细胞的DNA甲基化水平,下调参与褐黑素合成的基因Slc7a11的表达。其余参与褐黑素合成的基因(Slc45a2、MC1R及AGRP)的DNA甲基化虽也受到竞争性环境的影响,但未检测到其表达水平出现显著变化。竞争性环境暴露并未对受试鸟类的系统性氧化应激与氧化损伤产生影响,这提示机体或已激活了调控Slc7a11表达的保护性表观遗传机制。不过,研究未观察到受试鸟类的色素沉着表型发生改变,这可能缘于本次竞争性环境干预的持续时长较短或干预强度较低。丁胱亚磺酰亚胺处理并未对该表观遗传机制产生显著影响,这表明受试鸟类的抗氧化能力足以应对本次竞争性环境干预。综上,雄性斑胸草雀在暴露于竞争性环境时,会激活一种限制褐黑素合成的表观遗传机制,该机制或可有效规避竞争性互动所带来的机体损伤。
创建时间:
2023-06-28
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