Glycosylation in livers of newborn mice homozygous for a lethal deletion.

Abstract

Endogenous glycoprotein and lipid biosynthesis have been examined in slices of liver and other organs from normal and mutant mice homozygous for a perinatally lethal deletion in chromosome 7. Pronase digests of total glycoproteins, radioactively labeled with glucosamine, followed by Bio-Gel P-6 column chromatography of the resultant glycopeptides, indicate that glycosylation in mutant mouse liver is dramatically reduced compared to that of normal littermates. Pulse-chase experiments suggest that this reduction is not due to a processing event, but rather to reduced biosynthesis. In addition, a quantitative reduction of glycopeptides was observed in mutant livers, when the radioactive peaks from the Bio-Gel P-6 fractionation were pooled and analyzed on a Dowex 50 column, followed by separation on DE-52 columns. Analysis, by affinity chromatography, of radioactively labeled total lipids indicated that homozygous mutant and normal littermate livers have similar quantities of neutral and acidic lipids, including phosphatidylserine, phosphatidylinositol, cerebrosides, and phospholipids. Furthermore, the analysis of other organs indicates that the reduction of glycoprotein synthesis observed in the mutant liver is specific to this organ.