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Inhibition of Glycosphingolipid Biosynthesis Does Not Impair Growth or Morphogenesis of the Postimplantation Mouse Embryo
Author(s) -
Brigande John V.,
Platt Frances M.,
Seyfried Thomas N.
Publication year - 1998
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1998.70020871.x
Subject(s) - biology , embryo , biosynthesis , glycosphingolipid , morphogenesis , yolk , biochemistry , organogenesis , embryogenesis , yolk sac , ganglioside , lactosylceramide , microbiology and biotechnology , glycolipid , gene , ecology
Whole embryo culture (WEC) of organogenesis‐stage mouse embryos was adapted for glycosphingolipid (GSL) metabolic studies to evaluate the hypothesis that de novo GSL biosynthesis is a prerequisite for growth and morphogenesis of the early postimplantation embryo. WEC supports the growth and development of postimplantation mouse embryos to stages that are indistinguishable from those achieved in vivo. N ‐Butyldeoxygalactonojirimycin ( N B‐DGJ) is an N ‐alkylated imino sugar that specifically inhibits biosynthesis of all glucosylceramide‐based GSLs. N B‐DGJ inhibited glucosylceramide and lactosylceramide biosynthesis nearly completely and inhibited ganglioside biosynthesis ∼90% in both the embryo and visceral yolk sac. N B‐DGJ also significantly reduced total ganglioside content in both the embryo and visceral yolk sac as estimated by the cholera toxin immunooverlay technique. A shift in expression from the structurally simple to the structurally complex gangliosides was also observed in N B‐DGJ‐treated embryos and yolk sacs. Despite causing major changes in GSL biosynthesis and composition, N B‐DGJ had no effect on embryo viability, growth, or morphology. The findings suggest that de novo GSL biosynthesis may not be a prerequisite for the growth and morphogenesis of the organogenesis‐stage mouse embryo.