Gtl2/Dlk1印迹区域甲基化改变在酒精致雄性生殖损伤遗传中的作用研究

The teratogenic effects of ethanol exposure on male reproductive function have been well-documented. Increasing evidence suggests that chronic paternal alcohol consumption affects offspring development. However, few studies have been performed to examine whether these reproductive dysfuction can pass on to offspring. As of yet, the exact mechanistic basis of how paternal ethanol exposure contributes to offspring defects remains largely unclear. Researches have been shown that methylation alterations in imprinted genes may be related to the well-documented teratogenic effects of ethanol. Here, ethanol was administered intragastrically to male mice and the parameters of reproductive development were performed on their F0 - F2 generation. Based on our previous study, the imprinted genes (Dlk1/Gtl2) were chosen, and the degree of methylation and expression of imprinted genes (Dlk1/Gtl2) were assessed in the sperm of F0 - F2. Our results provide a possible epigenetic evidence for paternal ethanol exposure contributes to birth defect.

酒精影响男性生殖功能，过度饮酒可导致其性功能障碍并影响后代生长发育，但是否能导致生殖损伤的跨代遗传尚未见报道。迄今为止，父系酒精暴露致后代发育异常的机制尚未明了。研究表明，精子发生障碍与印迹异常有关，而印迹基因甲基化修饰对环境影响改变敏感且能够稳定遗传而成为当前研究热点。因此，本课题拟从前期已开展的F0代酒精暴露小鼠精子全基因组甲基化测序研究结果为基础，筛选出与生殖发育相关的印迹基因 , Dlk1/Gtl2 ，检测其差异甲基化位点(Differentially Methylated Region,DMR)甲基化状态在F0-F2代变化情况及其相关蛋白表达情况，并对相应后代雄性生殖发育进行评测。旨在为父系酒精暴露导致后代出生缺陷提供可能的表观遗传学机制。

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