“…Given that inner leaflet PtdEth promotes inactivation of Cdc42-GTP by its GAPs and/or GDI (Cherfils and Zeghouf, 2013), our results connect Gin4 action to modulation of the level of active Cdc42, an essential and pivotal regulator of cell polarity and morphogenesis (Etienne-Manneville, 2004;Bi and Park, 2012). Gin4, by negatively regulating Fpk1, inhibits the flippases under Fpk1 control, lowers inner leaflet PtdEth content, thus reducing PtdEth-stimulated GAP Cdc42 (Rga1 and Rga2; Saito et al, 2007) and/or Rho GDI (Rdi1; Das et al, 2012) function, thereby maintaining or increasing the concentration of PM-associated GTP-bound Cdc42 (Fig.…”