The kinase activity of pseudorabies virus US3 is required for modulation of the actin cytoskeleton.
Different viruses exploit the host cytoskeleton to facilitate replication and spread. The conserved US3 protein of the alphaherpesvirus pseudorabies virus induces actin stress fiber disassembly and formation of actin-containing cell projections, which are associated with enhanced intercellular virus spread. Proteins of members of other virus families, notably vaccinia virus F11L protein and human immunodeficiency virus Nef protein, induce actin rearrangements that are very similar to those induced by US3. Interestingly, unlike F11L and Nef, the US3 protein displays serine/threonine kinase activity. Here, we report that the kinase activity of pseudorabies virus US3 is absolutely required for its actin modulating activity. These data show that different viruses have developed independent mechanisms to induce very similar actin rearrangements.
Van den Broeke
Céline
C
Department of Virology, Parasitology, and Immunology, Ghent University, Belgium.
Deruelle
Matthias
M
Nauwynck
Hans J
HJ
Coller
Kelly E
KE
Smith
Gregory A
GA
Van Doorsselaere
Jan
J
Favoreel
Herman W
HW
D000199:Actins / Q000378:metabolism*; D000818:Animals; D002460:Cell Line; D003599:Cytoskeleton / Q000201:enzymology / Q000378:metabolism*; D011558:Herpesvirus 1, Suid / Q000201:enzymology* / Q000235:genetics*; D051379:Mice; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D011557:Pseudorabies / Q000473:pathology*; D014764:Viral Proteins / Q000378:metabolism*
D000199:Actins; D014764:Viral Proteins; D017346:Protein Serine-Threonine Kinases; C095207:US3 protein, Human herpesvirus 1