Oligosaccharides containing fucose linked α(1–3) and α(1–4) to N-acetylglucosamine cause decompaction of mouse morulae

Abstract

Two- to four-cell and eight-cell mouse embryos were incubated in various fucosylated and unfucosylated oligosaccharides, fucose binding protein, and fucosylated BSA. Compaction at the eight-cell stage was reversed by a mixture containing the oligosaccharides lacto- N-fucopentaose II (80–90%), in which fucose is linked α(1–4) to N-acetylglucosamine, and lacto- N-fucopentaose III (10–20%), in which fucose is linked α(1–3) to N-acetylglucosamine. Pure lacto- N-fucopentaose III (LNFP III) and 3-fucosyl lactose (containing fucose α(1–3)glucose) had a similar effect. All three molecules affected blastocyst formation. Various closely related fucosylated and unfucosylated oligosaccharides did not induce decompaction or inhibit blastocyst formation. The proportion of embryos incubated from the two- to four-cell stage in LNFP II/III which reached the eight-cell stage and formed blastocysts was reduced. Those which formed compact morulae subsequently decompacted. Precompact or early compacting eight-cell embryos incubated in LNFP II/III compacted normally but subsequently decompacted and failed to form blastocysts. Decompaction of eight-cell embryos in LNFP II/III occurred during a specific period of development (80–90 hr post-hCG) and was reversible up to 84–86 hr post-hCG, but not by 92 hr post-hCG. The period of sensitivity to LNFP II/III was associated with the decrease in the ability of calcium-free medium to cause decompaction. It appears that LNFP II/III interferes with a later calcium-independent phase of compaction and we propose that LNFP III and II inhibit an endogenous lectin-saccharide interaction between membranes involved in the stabilization of compaction.