Figure 2.

Control of cell shape and cytoskeletal dynamics by AKAP12. The downregulation of AKAP12 in v-Src–transformed NIH3T3 murine fibroblasts correlates with a transition from the polygonal morphology of parental NIH3T3 (top panel, middle) to a so-called fusiform morphology (top panel, left). In contrast, overexpression of AKAP12 via a Tet-OFF vector system³ causes cell flattening, the thinning of stress fibers, and the production of long filamentous (F) projections (top panel, right). The staining intensities in the top panel reflect relative levels of AKAP12. AKAP12 loss in MEF (bottom left) or in stellate mesangial cells due to treatment with antisense (ASN) AKAP12 oligonucleotides (bottom right) results in cell flattening marked by thickened, longitudinal stress fibers (“F-actin”) and increased numbers of focal adhesion plaques (“vinculin”).⁹