Elucidation of the Phenotypic Change on the Surface of Had-1 Cell, a Mutant Cell Line of Mouse FM3A Carcinoma Cells Selected by Resistance to Newcastle Disease Virus Infection

Abstract

Had-1, which was isolated from mouse FM3A carcinoma cells, was a non-permissive mutant cell line to Newcastle disease virus infection. Comparative study of the asparaginelinked sugar chains of the surface glycoproteins of the mutant and its parental cells revealed that galactosylation of the complex-type sugar chains is extensively reduced in the mutant. Assay of galactosyltransferase in the two cell lines, however, showed that the enzymatic activity in Had-1 cells is virtually identical to that in FM3A cells. Somatic cell hybridization analysis indicated that the mutant has the same defect as Chinese hamster ovary cell mutant Lec 8, which is deficient in UDP-galactose transport into Golgi vesicles.