Figure 2. Model of clathrin-mediated and Rho1-mediated endocytic pathways in yeast. Although many proteins contribute to CME which occurs at cortical actin patches (left), the model is simplified to display proteins that are critical for functional CME but that we have found are not required for endocytosis in the presence of high-copy components of the Rho1 pathway. CME components that are not required for Rho1-mediated endocytosis include coat proteins (clathrin and the adaptors Ent1, Ent2, Yap1801 and Yap1802), the Arp2/3-activating WASp homolog Las17, and the branched actin-bundling proteins Sac6/fimbrin and Scp1/transgelin. Components of the Rho1 pathway (right) do not localize to cortical actin patches, and are thought to act independently of the CME machinery. The Rho1 pathway ultimately promotes extension of tropomyosin-stabilized unbranched actin filaments through the activity of the formin Bni1, although how membrane deformation is achieved at sites of Rho1-mediated endocytosis is currently unclear.