Lipoproteins transport lipids from intestine and liver where they are absorbed and metabolized to peripheral tissues via the bloodstream. They contain core proteins (apo proteins) that bind various types of lipid, thus producing lipoprotein complexes of varying densities—very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL) after plasma lipoprotein electrophoresis. A disorder called abetalipoproteinemia (MIM*200100) was distinguished by its deficiency of the bands for very low density lipoproteins (VLDL) and low density lipoproteins (LDL) after plasma electrophoresis. Affected patients have ataxia (wide gait, incoordination), retinopathy (retinal degeneration with blindness), and myopathy (muscle weakness). VLDL and LDL contain the same apoB core protein, their different densities produced by association with different lipids, and apoB became good candidate for mutation in the disorder. Initial characterization of the apoB gene together with its mRNA and protein products demonstrated identical mRNA sizes in all tissues. Western blotting using antibody specific for the amino-terminus of apoB protein showed a 100-kDa species in liver and a 48-kDa species in intestine, as did antibody specific for the C-terminus of the 48-kDa intestinal protein. Molecular study of a patient with abetalipoproteinemia showed normal mRNA sizes, but 100-kDa peptide species were identified in both liver and intestine using the amino- or carboxy-terminus antibody probes. Which of the following processes is most likely deficient in this patient with apobetalipoproteinemia?