Complex asparagine-linked oligosaccharides in Mgat1-null embryos

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Abstract
To investigate the developmental role of complex N-linked oligosaccharides, we previously inactivated the mouse Mgat1 gene which encodes UDP-N-acetylglucosamine: α-3-D-mannoside β-1,2-N-acetylglucosaminyltransferase I (GlcNAc-TI). Mgat1-null embryos developed morphogenic abnormalities by embryonic day (E) 9.5 and failed to survive beyond E10.5. Prior to E8.5, mutant and wild-type embryos were phenotypically indistinguishable, raising the unexpected possibility that earlier embryonic development may not require complex N-glycans. We have now used in situ RNA hybridization to assess the temporal and spatial pattern of Mgat1 expression in normal embryos, and lectin histochemistry to determine whether Mgat1 -null embryos lack complex N-glycans at pre-E9.5 developmental stages. In situ RNA analysis indicated that Mgat1 transcripts normally increase dramatically between E7.0 and E9.5, 1–2 days prior to the death of mutant embryos. However, apparently normal levels of complex N-glycans were observed in E3.5 pre-implantation Mgat1-null embryos prior to declining to undetectable levels by E7.5. Complex N-glycans were not observed in E7.5-E9.5 Mgat1-null embryos with the notable exception of vesicular structures within cells of the visceral extra-embryonic endoderm, perhaps reflecting the ability of these cells to take up and transport maternally derived glycoproteins. Mgat1-null embryos appear to complete pre-implantation development in the presence of maternally derived complex N-glycaas, and may die at later stages, post E7.5, when a requirement for embyronically derived complex N-glycans arises.

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