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. 2001 Mar 5;152(5):867–876. doi: 10.1083/jcb.152.5.867

Figure 9.

Figure 9

Proposed involvement of PIP2 in stress-fiber assembly. The model is adapted from Maekawa et al. 1999 and Watanabe et al. 1999, and incorporates the finding that generation of a particular actin structure reflects the antagonistic as well as cooperative influences of multiple inputs. PIP5KI is regulated by multiple mechanisms. In this diagram, we focus on the Rho pathway, and show that the increase in PIP2 synthesis after PIP5KI overexpression is at least partly mediated through ROCK, because the ROCK inhibitor Y-27632 decreases PIP2 accumulation in cells. Our data suggest that inhibition may be due to a decrease in PI4P synthesis, although this is not yet established conclusively (?). The inhibitors used, and their sites of action, are indicated. The effect of PIP5KI overexpression on ADF/cofilin function was not determined, and hence the potential involvement of ADF/cofilin is denoted by a question mark. (Two-headed arrows) Reciprocal antagonistic actions, (black arrow) activation. The bar at the end of dashed line indicates inhibition after PIP5KI overexpression in CV1 cells. The dominance of signals to generate stress fibers in CV1 decreases the ability of the cells to ruffle their membrane, to form thin actin fibers, and to form actin comets.