Open AccessAn E2–F12 complex is required for intracellular enveloped virus morphogenesis during vaccinia infection
Author(s) -
Dodding Mark P.,
Newsome Timothy P.,
Collinson Lucy M.,
Edwards Ceri,
Way Michael
Publication year - 2009
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2009.01296.x
Subject(s) - vaccinia , biology , virology , morphogenesis , intracellular , virus , poxviridae , microbiology and biotechnology , genetics , gene , recombinant dna
Summary The vaccinia virus protein, F12, has been suggested to play an important role in microtubule‐based transport of intracellular enveloped virus (IEV). We found that GFP‐F12 is recruited to IEV moving on microtubules but is released from virus particles when they switch to actin‐based motility. In the absence of F12, although the majority of IEV remain close to their peri‐nuclear site of assembly, a small number of IEV still move with linear trajectories at speeds of 0.85 μm s −1 , consistent with microtubule transport. Using a recombinant virus expressing GST‐F12, we found that the viral protein E2 interacts directly with F12. In infected cells, GFP‐E2 is observed on moving IEV as well as in the Golgi region, but is not associated with actin tails. In the absence of E2L, IEV accumulate in the peri‐nuclear region and F12 is not recruited. Conversely, GFP‐E2 is not observed on IEV in the absence of F12. Ultra‐structural analysis of ΔE2L‐ and ΔF12L‐infected cells reveals that loss of either protein results in defects in membrane wrapping during IEV formation. We suggest that E2 and F12 function as a complex that is necessary for IEV morphogenesis prior to their microtubule‐based transport towards the plasma membrane.