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

Abstract:

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

journal_name

Nature

journal_title

Nature

authors

Frischknecht F,Moreau V,Röttger S,Gonfloni S,Reckmann I,Superti-Furga G,Way M

doi

10.1038/44860

keywords:

subject

Has Abstract

pub_date

1999-10-28 00:00:00

pages

926-9

issue

6756

eissn

0028-0836

issn

1476-4687

journal_volume

401

pub_type

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