Actin-based motility of vaccinia virus mimics receptor tyrosine kinase signalling.

摘要: Studies of the actin-based motility intracellular pathogens Listeria monocytogenes and Shigella flexneri have provided important insight into events occurring at leading edges motile cells. Like bacteria Shigella, vaccinia virus, a relative causative agent smallpox, uses to spread between In contrast or is dependent on an unknown phosphotyrosine protein, but underlying mechanism remains obscure. Here we show that phosphorylation tyrosine 112 in viral protein A36R by Src-family kinases essential for vaccinia. Tyrosine results direct interaction with adaptor Nck recruitment Ena/VASP family member N-WASP site actin assembly. We also are virus. suggest virus spreads mimicking signalling pathways normally involved polymerization plasma membrane.