CHC22 clathrin recruitment to the early secretory pathway requires two-site interaction with SNX5 and p115.

The two clathrin isoforms, CHC17 and CHC22, mediate separate intracellular transport routes. CHC17 performs endocytosis and housekeeping membrane traffic in all cells. CHC22, expressed most highly in skeletal muscle, shuttles the glucose transporter GLUT4 from the ERGIC (endoplasmic-reticulum-to-Golgi intermediate compartment) directly to an intracellular GLUT4 storage compartment (GSC), from where GLUT4 can be mobilized to the plasma membrane by insulin.

Fluorescence Recovery After Photobleaching to Study the Dynamics of Membrane-Bound Proteins In Vivo Using the Drosophila Embryo.

The epithelial-to-mesenchymal transition is a highly dynamic cell process and tools such as fluorescence recovery after photobleaching (FRAP), which allow the study of rapid protein dynamics, enable the following of this process in vivo. This technique uses a short intense pulse of photons to disrupt the fluorescence of a tagged protein in a region of a sample. The fluorescent signal intensity after this bleaching is then recorded and the signal recovery used to provide an indicator of the dynamics of the protein of interest.

Arf6 determines tissue architecture by stabilizing intercellular adhesion.

Correct cell shape is indispensable for tissue architecture, with cell shape being determined by cortical actin and surface adhesion. The role of adhesion in remodelling tissue is to counteract the deformation of cells by force, resulting from actomyosin contractility, and to maintain tissue integrity. The dynamics of this adhesion are critical to the processes of cell shape formation and maintenance.

Interplay between actomyosin and E-cadherin dynamics regulates cell shape in the embryonic epidermis.

Precise regulation of cell shape is vital for building functional tissues. Here, we study the mechanisms that lead to the formation of highly elongated anisotropic epithelial cells in the epidermis. We demonstrate that this cell shape is the result of two counteracting mechanisms at the cell surface that regulate the degree of elongation: actomyosin, which inhibits cell elongation downstream of RhoA (Rho1 in ) and intercellular adhesion, modulated via clathrin-mediated endocytosis of E-cadherin (encoded by in flies), which promotes cell elongation downstream of the GTPase Arf1 (Arf79F in ).