Figure 4. Model of the effects of paxillin and paxillin mutants on lamellipodia formation in square cells. The square, representing a shape-constrained cell, is divided into four quadrants, which correspond to paxillin−/−, paxillin+/+, paxN and paxC cell conditions. In control (pax+) cells (top right), paxillin may bind cytosolic or membrane-bound Rac-activating complexes and recruit them to focal adhesion (FA) sites. For example, upon PDGF receptor activation paxillin could bind Pkl-PIX-PAK complexes containing Arf6-GTP and Rac-GTP and deliver them to corner regions to promote localized lamellipodia formation. In paxillin−/− cells (top left), some active Rac complexes may drive limited, non-localized lamellipodia extension at the cell periphery, but delivery from endosomal compartments to the plasma membrane may be impaired. The C-terminal paxC fragment (bottom left) could compete with Hic-5, PTP-PEST or Rac inhibiting proteins, promoting enhanced lamellipodia formation even in the absence of growth factors. Conversely, the N-terminal paxN fragment (bottom right) could sequester Rac-activating proteins and lamellipodia machinery in the cytosol. The small, spiky protrusions in these cells could be driven by Cdc42 or RhoA instead of by Rac.