OLIGOSACCHARIDES CONTAINING FUCOSE LINKED ALPHA(1-3) AND ALPHA(1-4) TO N-ACETYLGLUCOSAMINE CAUSE DECOMPACTION OF MOUSE MORULAE

Two- to 4-cell and 8-cell mouse embryos were incubated in various fucosylated and unfucosylated oligosaccharides, fucose binding protein and fucosylated BSA [bovine serum albumin]. Compaction at the 8-cell stage was reversed by a mixture containing the oligosaccharides lacto-N-fucopentaose II (80-90%), in which fucose is linked .alpha.(1-4) to N-acetylglucosamine, and lacto-N-fucopentaose III (10-20%), in which fucose is linked .alpha.(1-3) to N-acetylglucosamine. Pure lacto-N-fucopentaose III (LNFP III) and 3-fucosyl lactose (containing fucose .alpha.(1-3)glucose) had a similar effect. All 3 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 2-4 cell stage in LNFP II/III which reached the 8-cell stage and formed blastocysts was reduced. Those which formed compact morulae subsequently decompacted. Precompact or early compacting 8 cell embryos incubated in LNFP II/III compacted normally but subsequently decompacted and failed to form blastocysts. Decompaction of 8-cell embryos in LNFP II/III occurred during a specific period of development (80-90 h post-hCG) and was reversible up to 84-86 h post-hCG, but not by 92 h post-hCG. The period of sensitivity to LNPF II/III was associated with the decrease in the ability of Ca-free medium to cause decompaction. LNFP II/III evidently interferes with a later Ca-independent phase of compaction and it is proposed that LNFP III and II inhibit an endogenous lectin-saccharide interaction between membranes involved in the stabilization of compaction.