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多代酸化缓解对无性单巢轮虫端点、抗氧化防御、DNA 损伤反应和表观遗传修饰的影响。

Multigenerational Mitigating Effects of Ocean Acidification on Endpoints, Antioxidant Defense, DNA Damage Response, and Epigenetic Modification in an Asexual Monogonont Rotifer.

机构信息

Department of Biological Science, College of Science, Sungkyunkwan University, Suwon 16419, South Korea.

Key Laboratory of the Ministry of Education for Coastal and Wetland Ecosystems/College of the Environment and Ecology, Xiamen University, Xiamen 361102, China.

出版信息

Environ Sci Technol. 2020 Jul 7;54(13):7858-7869. doi: 10.1021/acs.est.0c01438. Epub 2020 Jun 12.

Abstract

Ocean acidification (OA) is caused by changes in ocean carbon chemistry due to increased atmospheric CO and is predicted to have deleterious effects on marine ecosystems. While the potential impacts of OA on many marine species have been studied, the multigenerational effects on asexual organisms remain unknown. We found that low seawater pH induced oxidative stress and DNA damage, decreasing growth rates, fecundity, and lifespans in the parental generation, whereas deleterious effects on endpoints in F1 and F2 offspring were less evident. The findings suggest that multigenerational adaptive effects play a role in antioxidant abilities and other defense mechanisms. OA-induced DNA damage, including double-strand breaks (DSBs), was fully repaired in F1 offspring of parents exposed to OA for 7 days, indicating that an adaptation mechanism may be the major driving force behind multigenerational adaptive effects. Analysis of epigenetic modification in response to OA involved examination of histone modification of DNA repair genes and a chromatin immunoprecipitation assay, as has no methylation pattern for CpG in its genome. We conclude that DSBs, DNA repair, and histone modification play important roles in multigenerational plasticity in response to OA in an asexual monogonont rotifer.

摘要

海洋酸化(OA)是由于大气 CO 增加导致海洋碳化学变化引起的,预计会对海洋生态系统产生有害影响。虽然 OA 对许多海洋物种的潜在影响已经得到研究,但无性生物的多代影响仍不清楚。我们发现,低海水 pH 值会引起氧化应激和 DNA 损伤,从而降低亲代的生长速度、繁殖力和寿命,而对 F1 和 F2 后代的终点的有害影响则不那么明显。研究结果表明,多代适应效应在抗氧化能力和其他防御机制中发挥作用。在父母暴露于 OA 7 天后,F1 后代中的 OA 诱导的 DNA 损伤,包括双链断裂(DSBs),已被完全修复,这表明适应机制可能是多代适应效应的主要驱动力。针对 OA 的表观遗传修饰分析涉及对 DNA 修复基因的组蛋白修饰的分析,以及染色质免疫沉淀测定,因为其基因组中没有 CpG 的甲基化模式。我们得出结论,在无性单沟轮虫中,DSBs、DNA 修复和组蛋白修饰在对 OA 的多代可塑性中发挥重要作用。

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