Sunahara S, Nakamura K, Nakao K, Gondo Y, Nagata Y, Katsuki M
Division of DNA Biology and Embryo Engineering, CREST, Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Tokyo, Minato-ku, 108-8639, Japan.
Biochem Biophys Res Commun. 2000 Feb 16;268(2):590-5. doi: 10.1006/bbrc.2000.2189.
Imprinted genes harbor discrete regions which are differentially methylated in gametes; usually the final differential methylation patterns in adults are established during embryogenesis through modifications of the initial methylation patterns in gametes. Previous reports have shown that a 200-bp region termed region II within the CpG island of the mouse imprinted U2afbp-rs gene is methylated in oocytes but not in sperm, suggesting that this region is a center for the propagation of methylated CpGs on the maternal allele and is also a candidate for an imprinting control element. To determine whether region II is required for the imprinted methylation of this gene at the endogenous locus, we generated mice carrying a deletion of this region. We herein show that parental methylation differences still exist in the CpG island on the region II-deleted allele. These findings suggest that region II is dispensable for the imprinted methylation of the U2afbp-rs gene.
印记基因含有在配子中差异甲基化的离散区域;通常,成体中的最终差异甲基化模式是在胚胎发育过程中通过对配子中初始甲基化模式的修饰而建立的。先前的报道表明,小鼠印记基因U2afbp-rs的CpG岛内一个名为区域II的200bp区域在卵母细胞中甲基化,但在精子中未甲基化,这表明该区域是母本等位基因上甲基化CpG传播的中心,也是印记控制元件的候选区域。为了确定区域II是否是该基因在内源位点进行印记甲基化所必需的,我们构建了携带该区域缺失的小鼠。我们在此表明,在区域II缺失的等位基因的CpG岛上,亲本甲基化差异仍然存在。这些发现表明,区域II对于U2afbp-rs基因的印记甲基化是可有可无的。