Conservation of the architecture of the Golgi apparatus related to a differential organization of microtubules in polykaryocytes induced by syn- mutants of herpes simplex virus 1.

Infection of Vero and HEp-2 but not of 143TK- cells with herpes simplex virus 1 results in fragmentation and dispersal of the Golgi apparatus. Concurrently, in all three infected cell lines the microtubular network is disrupted, suggesting that the disruption of microtubules is essential but not sufficient to induce the fragmentation of the Golgi apparatus. We now report the following: (i) In polykaryocytes formed in Vero cells infected with HSV-1 syn- mutant viruses, intact Golgi stacks were readily detected by electron microscopy. These aggregated in the center of large polykaryocytes. (ii) The distribution of viral glycoprotein D, examined in both fixed and nonfixed cells, appeared to match the distribution of the Golgi stacks, suggesting that the aggregated Golgi stacks funnel viral glycoproteins and viral particles to a limited region of the plasma membrane of the polykaryocytes rather than directing exocytic flow in a more dispersed fashion as seen in syn+ virus-infected cells exhibiting fragmented and dispersed Golgi. (iii) In most polykaryocytes, the microtubules formed parallel bundles extending along the axis of recruitment of new cells. (iv) Fragmentation of the microtubules at the periphery of the cell near the plasma membrane was observed in untreated or cycloheximide-treated cells 2 h after infection with syn- virus HSV-1(MP) or syn+ HSV-1(mP) but not in mock-infected cells. These observations suggest that peripheral depolymerization is initiated at the time of infection and that a factor which determines the syn- or syn+ phenotype is whether the microtubular network regenerates concomitant with cell fusion or reorganizes to form a collapsed network surrounding nuclei of syn+ infected cells.