期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2003
卷号：100
期号：11
页码：6493-6498
DOI：10.1073/pnas.1031670100
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Polymerizing networks of actin filaments generate force for a variety of movements in living cells, including protrusion of filopodia and lamellipodia, intra- and intercellular motility of certain bacterial and viral pathogens, and motility of endocytic vesicles and other membrane-bound organelles. During actin-based motility, coexisting populations of actin filaments exert both pushing and retarding forces on the moving cargo. To examine the distribution and magnitude of forces generated by actin, we have developed a model system where large artificial lipid vesicles coated with the protein ActA from the bacterial pathogen Listeria monocytogenes are propelled by actin polymerization in cytoplasmic extract. We find that motile vesicles associated with actin comet tails are significantly deformed due to an inward compression force exerted by actin polymerization orthogonal to the direction of motion, which is >10-fold greater in magnitude than the component of the force exerted in the direction of motion. Furthermore, there is a spatial segregation of the pushing and retarding forces, such that pushing predominates along the sides of the vesicle, although retarding forces predominate at the rear. We estimate that the total net (pushing minus retarding) force generated by the actin comet tail is {approx}0.4-4 nN. In addition, actin comet tail formation is associated with polarization of the ActA protein on the fluid vesicle surface, which may reinforce the persistence of unidirectional motion by helping to maintain a persistent asymmetry of actin filament density.
