Erasure of DNA methylation in rat fetal germ cells is sex-specific and sensitive to maternal high-fat diet.

IF 1.8 4区医学 Q3 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH

Journal of Developmental Origins of Health and Disease Pub Date : 2024-09-26 DOI:10.1017/S2040174424000230

R El Omri-Charai, A Rwigemera, I Gilbert, A Langford, C Robert, D M Sloboda, S McGraw, G Delbes

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Abstract

In mammals, DNA methylation (DNAme) erasure and reinstatement during embryo development and germline establishment are sensitive to the intrauterine environment. Maternal intake of a high-fat diet (HFD), associated with excessive gestational weight gain, has transgenerational effects on offspring health, which may be mediated by changes in DNAme in the germline. Here, we tested the impact of a maternal HFD on embryonic germline DNAme erasure using a rat strain that expresses green fluorescent protein specifically in germ cells. DNAme was analysed by methyl-seq capture in germ cells collected from male and female F1 gonads at gestational day 16. Our data show that although HFD induced global hypomethylation in both sexes, DNAme erasure in female germ cells was more advanced compared to male germ cells. The delay in DNAme erasure in males and the greater impact of HFD suggest that male germ cells are more vulnerable to alterations by exogenous factors.

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大鼠胎儿生殖细胞中DNA甲基化的消除具有性别特异性，并对母体高脂肪饮食敏感。

在哺乳动物中，胚胎发育和种系建立过程中DNA甲基化（DNAme）的消除和恢复对宫内环境很敏感。母体摄入高脂肪饮食（HFD）会导致妊娠期体重增加过多，从而对后代的健康产生跨代影响，而这种影响可能是通过种系中 DNAme 的变化介导的。在这里，我们使用一种能在生殖细胞中特异性表达绿色荧光蛋白的大鼠品系，测试了母体高脂肪饮食对胚胎生殖细胞 DNAme 清除的影响。我们通过甲基序列捕获技术分析了在妊娠第16天从雄性和雌性F1性腺中采集的生殖细胞中的DNAme。我们的数据显示，虽然高频分解雌雄性腺细胞都会诱导全局低甲基化，但与雄性生殖细胞相比，雌性生殖细胞的DNAme清除更快。雄性生殖细胞DNAme清除的延迟和HFD的更大影响表明，雄性生殖细胞更容易受到外源因素的改变。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Developmental Origins of Health and Disease PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH-

CiteScore

3.80

自引率

0.00%

发文量

145

审稿时长

6-12 weeks

期刊介绍： JDOHaD publishes leading research in the field of Developmental Origins of Health and Disease (DOHaD). The Journal focuses on the environment during early pre-natal and post-natal animal and human development, interactions between environmental and genetic factors, including environmental toxicants, and their influence on health and disease risk throughout the lifespan. JDOHaD publishes work on developmental programming, fetal and neonatal biology and physiology, early life nutrition, especially during the first 1,000 days of life, human ecology and evolution and Gene-Environment Interactions. JDOHaD also accepts manuscripts that address the social determinants or education of health and disease risk as they relate to the early life period, as well as the economic and health care costs of a poor start to life. Accordingly, JDOHaD is multi-disciplinary, with contributions from basic scientists working in the fields of physiology, biochemistry and nutrition, endocrinology and metabolism, developmental biology, molecular biology/ epigenetics, human biology/ anthropology, and evolutionary developmental biology. Moreover clinicians, nutritionists, epidemiologists, social scientists, economists, public health specialists and policy makers are very welcome to submit manuscripts. The journal includes original research articles, short communications and reviews, and has regular themed issues, with guest editors; it is also a platform for conference/workshop reports, and for opinion, comment and interaction.