Skip to main content
. 2010 Oct 20;85(1):568–581. doi: 10.1128/JVI.01611-10

FIG. 9.

FIG. 9.

HSV-1 and PRV US3 kinases drive nuclear retention of matrin 3 during infection. Shown are immunofluorescence analyses of MRC-5 cells that were either mock infected (A) or infected with HSV-1 (B), HSV.US3.5 (C), HSV.ΔUS3 (D), PRV (E), or PRV.ΔUS3 (F) at an MOI of 5. Cells were fixed with 4% paraformaldehyde 18 h (HSV) or 11 h (PRV) postinfection; then they were immunostained either with a rabbit α-matrin 3 antibody (A to F, panels i), detected with α-rabbit Alexa Fluor 546 (HSV) or α-rabbit Alexa Fluor 555 (PRV); with mouse α-HSV ICP4 (A to D, panels iii) (magenta), detected with α-mouse Alexa Fluor 647; or with goat α-PRV UL34 (E and F, panels iii) (magenta), detected with α-goat Alexa Fluor 647. GFP-US3.5 expression or US3 promoter activity in HSV.ΔUS3- and PRV.ΔUS3-infected cells was determined using GFP autofluorescence (A to F, panels ii) (green). The merge images (A to F, panels iv) are overlays of matrin 3 (gray) and nuclei stained with Hoechst dye (blue). Fluorescence images were taken using a 60× objective.