The length of vesicular stomatitis virus particles dictates a need for actin assembly during clathrin-dependent endocytosis.

ABSTRACT: Microbial pathogens exploit the clathrin endocytic machinery to enter host cells. Vesicular stomatitis virus (VSV), an enveloped virus with bullet-shaped virions that measure 70 x 200 nm, enters cells by clathrin-dependent endocytosis. We showed previously that VSV particles exceed the capacity of typical clathrin-coated vesicles and instead enter through endocytic carriers that acquire a partial clathrin coat and require local actin filament assembly to complete vesicle budding and internalization. To understand why the actin system is required for VSV uptake, we compared the internalization mechanisms of VSV and its shorter (75 nm long) defective interfering particle, DI-T. By imaging the uptake of individual particles into live cells, we found that, as with parental virions, DI-T enters

SUBMITTER: Cureton DK 

PROVIDER: S-EPMC2947997 | biostudies-literature | 2010 Sep

REPOSITORIES: biostudies-literature