Transition from van-der-Waals to H Bonds dominated Interaction in n-Propanol physisorbed on Graphite

Multilayer sorption isotherms of 1-propanol on graphite have been measured by means of high-resolution ellipsometry within the liquid regime of the adsorbed film for temperatures ranging from 180 to 260 K. In the first three monolayers the molecules are oriented parallel to the substrate and the growth is roughly consistent with the Frenkel-Halsey-Hill-model (FHH) that is obeyed in van-der-Waals systems on strong substrates. The condensation of the fourth and higher layers is delayed with respect to the FHH-model. The fourth layer is actually a bilayer. Furthermore there is indication of a wetting transition. The results are interpreted in terms of hydrogen-bridge bonding within and between the layers.Comment: 4 pages, 3 figure

Cortactin Promotes Migration and Platelet-derived Growth Factor-induced Actin Reorganization by Signaling to Rho-GTPases

Dynamic actin rearrangements are initiated and maintained by actin filament nucleators, including the Arp2/3-complex. This protein assembly is activated in vitro by distinct nucleation-promoting factors such as Wiskott-Aldrich syndrome protein/Scar family proteins or cortactin, but the relative in vivo functions of each of them remain controversial. Here, we report the conditional genetic disruption of murine cortactin, implicated previously in dynamic actin reorganizations driving lamellipodium protrusion and endocytosis. Unexpectedly, cortactin-deficient cells showed little changes in overall cell morphology and growth. Ultrastructural analyses and live-cell imaging studies revealed unimpaired lamellipodial architecture, Rac-induced protrusion, and actin network turnover, although actin assembly rates in the lamellipodium were modestly increased. In contrast, platelet-derived growth factor-induced actin reorganization and Rac activation were impaired in cortactin null cells. In addition, cortactin deficiency caused reduction of Cdc42 activity and defects in random and directed cell migration. Reduced migration of cortactin null cells could be restored, at least in part, by active Rac and Cdc42 variants. Finally, cortactin removal did not affect the efficiency of receptor-mediated endocytosis. Together, we conclude that cortactin is fully dispensable for Arp2/3-complex activation during lamellipodia protrusion or clathrin pit endocytosis. Furthermore, we propose that cortactin promotes cell migration indirectly, through contributing to activation of selected Rho-GTPases