Extended Data Fig. 8: The DSC2 intracellular domain is dispensable for EBV infection, Related to Fig. 4.
From: Epstein–Barr virus exploits desmocollin 2 as the principal epithelial cell entry receptor
a, DSC2 expression was detected in NP69 cells with DSC2 wild type (WT) or mutant (deleted intracellular domain, ΔIC) by western blot. b, Deletion of DSC2 intracellular domain (ΔIC) didn’t affect EBV infection. NP69 cells with DSC2 wild type (WT) or mutant (deleted intracellular domain, ΔIC) were infected with EBV through cell-cell contact or cell-free EBV. EBV infection efficiency was determined by fluorescence microscope. c, d, EBV gHgL interacted with DSC2 through its 1st and 2nd cadherin-like repeats in NOK and NP69 cells. FLAG tagged gH21-678gL were expressed with mCherry tagged wt or mutant (with deletion of EC1-2) DSC2 in NOK (c) and NP69 (d) cells. The anti-FLAG antibody M2 was used to immunoprecipitate EBV gHgL and the associated complex. WT or mutant DSC2 (ΔEC1-2) was detected by mCherry antibody in western blots. e, Expression of WT or mutant DSC2 in YCCEL1 and NP69 cells determined by western blotting. GAPDH served as an internal control. Represented images from two independent experiments. Scale bars: 150 μm.
