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Fig. 7. The hollowing of NuMA is blocked by PAA. HEp-2 cells mock infected (A) or infected with HSV-1 in the absence (E) or presence (I) of PAA were pre-extracted with 0.1% Triton X-100 prior to fixation at 12 hours post infection. hollowing of NuMA was observed in normal, infected cells (arrow) (E). In cells infected in the presence of PAA, the localisation of NuMA (I) was the same as that in mock-infected cells (A), suggesting that viral DNA synthesis was important for the relocalisation and solubilisation of NuMA. In Vero cells that were transiently transfected with RFP-NuMA, infected with F-VP26/GFP, and then fixed at 7 hours post infection, the centre of the nucleus (where VP26-GFP had accumulated) lacked RFP-NuMA (F-H). In PAA-treated infected cells, however, the pattern of RFP-NuMA was similar to uninfected cells (B-D) at 7 hours post infection (data not shown). Even at 20 hours post infection, most of RFP-NuMA remained in the central parts of the nucleus (J-L).
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