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Actin filament elongation in Arp2/3-derived networks is controlled by three distinct mechanisms.

Dev Cell. 2013 Jan 28;24(2):182-95. Epub 2013 Jan 17
Alphée Michelot 1 , Alexandre Grassart , Voytek Okreglak , Michael Costanzo , Charles Boone , David G Drubin
Alphée Michelot 1 , Alexandre Grassart , Voytek Okreglak , Michael Costanzo , Charles Boone , David G Drubin
+ et al

[No authors listed]

Author information
  • 1 Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3202, USA.

摘要


Spatial and temporal control of actin filament barbed end elongation is crucial for force generation by actin networks. In this study, genetics, cell biology, and biochemistry were used to reveal three complementary mechanisms that regulate actin filament barbed end elongation in Arp2/3-derived networks. Aip1 inhibits elongation of aged ADP-actin filaments decorated with cofilin and, together with capping protein (CP), maintains a high level of assembly-competent actin species. We identified Abp1 and Aim3 as two additional proteins that work together to inhibit barbed end elongation. Abp1/Aim3 collaborates with CP to control elongation of newly assembled ATP-actin filaments to organize filament polarity within actin networks. Thus, three distinct mechanisms control filament elongation in different regions of Arp2/3 networks, maintaining pools of assembly-competent actin species while ensuring proper filament polarity and facilitating force production.