M. dunni and FerrD2 cells express the same dCAT-1 receptor, but these cells differ in their relative infectivity by MoMLV and Spl574, and they produce syncytia in response to different virus isolates. One possible explana- tion for these differences is that CAT-1 may undergo different post-translational modification in the two cell lines. It has been shown that resistance of M. dunni cells to MoMLV infection is reduced by treatment with the inhibitor of glycosylation, tunicamycin (Tu) [10] . The involvement of glycosylation is also suggested by the observation that the CAT-1 glycosylation patterns differ in transfected MA139 and M. dunni cells ( Fig. 1B ; lanes e,f).