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首页> 外文期刊>Molecular and Cellular Biology >Normal Embryonic and Germ Cell Development in Mice Lacking α1,3-Fucosyltransferase IX (Fut9) Which Show Disappearance of Stage-Specific Embryonic Antigen 1
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Normal Embryonic and Germ Cell Development in Mice Lacking α1,3-Fucosyltransferase IX (Fut9) Which Show Disappearance of Stage-Specific Embryonic Antigen 1

机译：缺少阶段特定胚胎抗原1的小鼠缺少α1,3-岩藻糖基转移酶IX（Fut9）的正常胚胎和生殖细胞发育。

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Stage-specific embryonic antigen 1 (SSEA-1), an antigenic epitope defined as a Lewis x carbohydrate structure, is expressed during the 8-cell to blastocyst stages in mouse embryos and in primordial germ cells, undifferentiated embryonic stem cells, and embryonic carcinoma cells. For many years, SSEA-1 has been implicated in the development of mouse embryos as a functional carbohydrate epitope in cell-to-cell interaction during morula compaction. In a previous study, α1,3-fucosyltransferase IX (Fut9) exhibited very strong activity for the synthesis of Lewis x compared to other α1,3-fucosyltransferases in an in vitro substrate specificity assay. Fut4 and Fut9 transcripts were expressed in mouse embryos. The Fut9 transcript was detected in embryonic-day-13.5 gonads containing primordial germ cells, but the Fut4 transcript was not. In order to identify the role of SSEA-1 and determine the key enzyme for SSEA-1 synthesis in vivo, we have generated Fut9-deficient (Fut9?/?) mice. Fut9?/? mice develop normally, with no gross phenotypic abnormalities, and are fertile. Immunohistochemical analysis revealed an absence of SSEA-1 expression in early embryos and primordial germ cells of Fut9?/? mice. Therefore, we conclude that expression of the SSEA-1 epitope in the developing mouse embryo is not essential for embryogenesis in vivo.
机译：阶段特异性胚胎抗原1（SSEA-1）是一种定义为Lewis x碳水化合物结构的抗原表位，在小鼠胚胎和原始生殖细胞，未分化的胚胎干细胞和胚胎癌的8细胞到胚泡阶段表达细胞。多年来，SSEA-1与桑致密化过程中细胞间相互作用中功能性碳水化合物表位相关，参与了小鼠胚胎的发育。在以前的研究中，在体外底物特异性测定中，与其他α1,3-岩藻糖基转移酶相比，α1,3-岩藻糖基转移酶IX（Fut9）对Lewis x的合成表现出非常强的活性。 Fut4 和 Fut9 转录本在小鼠胚胎中表达。在包含原始生殖细胞的胚胎天13.5性腺中检测到 Fut9 转录本，但未检测到 Fut4 转录本。为了确定SSEA-1的作用并确定体内SSEA-1合成的关键酶，我们已经生成了Fut9缺陷型（Fut9 ？/？）小鼠。 Fut9 ？/？小鼠发育正常，没有明显的表型异常，并且可育。免疫组织化学分析显示Fut9 ？/？小鼠的早期胚胎和原始生殖细胞中没有SSEA-1表达。因此，我们得出结论，在发育中的小鼠胚胎中SSEA-1表位的表达对于体内胚胎发生不是必需的。

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