1887

Abstract

The PML protein is one of the components of ND10, nuclear matrix-associated structures which undergo rapid disintegration at the onset of herpes simplex virus type 1 (HSV-1) infection. This disruption event has been frequently visualized in immunofluorescence assays using the anti-PML mouse monoclonal antibody PG-M3. This antibody was surprisingly found to also stain nuclear virus replication compartments when employed at higher concentrations. This was shown to be due to an unexpected cross-reactivity of the PG-M3 antibody with the HSV-1 immediate early protein ICP4, a known component of replication compartments. The sequences of ICP4 recognized by PG-M3 were found to map to the extreme amino-terminal end of the protein, which includes a 21 amino acid segment that is partially homologous to the peptide of PML that was used to make PG-M3. These results suggest that PG-M3 may no longer represent an appropriate antibody for use in visualizing the fate of PML and ND10 during HSV-1 infection.

Loading

Article metrics loading...

/content/journal/jgv/10.1099/0022-1317-81-7-1773
2000-07-01
2024-12-13
Loading full text...

Full text loading...

/deliver/fulltext/jgv/81/7/0811773a.html?itemId=/content/journal/jgv/10.1099/0022-1317-81-7-1773&mimeType=html&fmt=ahah

References

  1. Burkham, J., Coen, D. M. & Weller, S. K. (1998). ND10 protein PML is recruited to herpes simplex virus type 1 prereplicative sites and replication compartments in the presence of viral DNA polymerase.Journal of Virology 72, 10100-10107. [Google Scholar]
  2. de Bruyn Kops, A. & Knipe, D. M. (1988). Formation of DNA replication structures in herpes virus-infected cells requires a viral DNA binding protein.Cell 55, 857-868.[CrossRef] [Google Scholar]
  3. DeLuca, N. A. & Schaffer, P. A. (1988). Physical and functional domains of the herpes simplex virus transcriptional regulatory protein ICP4.Journal of Virology 62, 732-743. [Google Scholar]
  4. Everett, R. D. (1999). A surprising role for the proteasome in the regulation of herpesvirus infection.Trends in Biochemical Sciences 24, 293-295.[CrossRef] [Google Scholar]
  5. Everett, R. D. & Maul, G. G. (1994). HSV-1 IE protein Vmw110 causes redistribution of PML.EMBO Journal 13, 5062-5069. [Google Scholar]
  6. Everett, R. D., Freemont, P., Saitoh, H., Dasso, M., Orr, A., Kathoria, M. & Parkinson, J. (1998). The disruption of ND10 during herpes simplex virus infection correlates with the Vmw110- and proteasome-dependent loss of several PML isoforms.Journal of Virology 72, 6581-6591. [Google Scholar]
  7. Flenghi, L., Fagioli, M., Tomassoni, L., Pileri, S., Gambacorta, M., Pacini, R., Grignani, F., Casini, T., Ferrucci, P. F., Martelli, M. F., Pelicci, P. G. & Falini, B. (1995). Characterization of a new monoclonal antibody (PG-M3) directed against the aminoterminal portion of the PML gene product: immunocytochemical evidence for high expression of PML proteins on activated macrophages, endothelial cells, and epithelia.Blood 85, 1871-1880. [Google Scholar]
  8. Ishov, A. M. & Maul, G. G. (1996). The periphery of nuclear domain 10 (ND10) as site of DNA virus deposition.Journal of Cell Biology 134, 815-826.[CrossRef] [Google Scholar]
  9. Lukonis, C. J., Burkham, J. & Weller, S. K. (1997). Herpes simplex virus type 1 prereplicative sites are a heterogeneous population: only a subset are likely to be precursors to replication compartments.Journal of Virology 71, 4771-4781. [Google Scholar]
  10. McGeoch, D. J., Dolan, A., Donald, S. & Brauer, D. H. (1986). Complete DNA sequence of the short repeat region in the genome of herpes simplex virus type 1.Nucleic Acids Research 14, 1727-1745.[CrossRef] [Google Scholar]
  11. Maul, G. G. & Everett, R. D. (1994). The nuclear location of PML, a cellular member of the C3HC4 zinc-binding domain protein family, is rearranged during herpes simplex virus infection by the C3HC4 viral protein ICP0.Journal of General Virology 75, 1223-1233.[CrossRef] [Google Scholar]
  12. Maul, G. G., Guldner, H. H. & Spivack, J. G. (1993). Modification of discrete nuclear domains induced by herpes simplex virus type-1 immediate early gene-1 product (ICP0).Journal of General Virology 74, 2679-2690.[CrossRef] [Google Scholar]
  13. Maul, G. G., Ishov, A. M. & Everett, R. D. (1996). Nuclear domain 10 as preexisting potential replication start sites of herpes simplex virus type-1.Virology 217, 67-75.[CrossRef] [Google Scholar]
  14. Quinlan, M. P., Chen, L. B. & Knipe, D. M. (1984). The intranuclear location of a herpes simplex virus DNA-binding protein is determined by the status of viral DNA replication.Cell 36, 857-868.[CrossRef] [Google Scholar]
  15. Spatz, S. J., Nordby, E. C. & Weber, P. C. (1996). Mutational analysis of ICP0R, a transrepressor protein created by alternative splicing of the ICP0 gene of herpes simplex virus type 1.Journal of Virology 70, 7360-7370. [Google Scholar]
  16. Sternsdorf, T., Grotzinger, T., Jensen, K. & Will, H. (1997). Nuclear dots: actors on many stages.Immunobiology 198, 307-331.[CrossRef] [Google Scholar]
/content/journal/jgv/10.1099/0022-1317-81-7-1773
Loading
/content/journal/jgv/10.1099/0022-1317-81-7-1773
Loading

Data & Media loading...

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error