How does invagination and maturation of the clathrin-coated vesicle occur? Clathrin-coated vesicle maturation incorporates the activities of a range of proteins. Actin, myosin and WASP all have important roles in the formation and stabilization of clathrin-coated pits (CCPs) [1][2][3]. Evidence also suggests that F-actin [...]
How does the clathrin-coated vesicle neck narrow? In the final stages of clathrin-coated vesicle (CCV) formation, Phosphatidylinositol-4,5-bisphosphate (PIP2) undergoes a dephosphorylation by phosphatases such as synaptojanin 1 (Synj1) [1]. Not only does this inhibit PIP2’s signal transduction capabilities and ensures that the adaptor proteins [...]
What is membrane curvature? Membrane curvature refers to the physical bending of membranes to accommodate various cell morphology changes as well as the formation of membrane-bound transport intermediates like spherical vesicles or tubules. As membranes are inelastic and resistant to spontaneous bending, membrane curvature [...]
What is Membrane Trafficking? Membrane trafficking encompasses the wide variety of processes that go into the movement of cargo (typically proteins, pathogens and other macromolecules) using membrane bound transport vesicles. This transport can take place within different organelles in the same cell, or across [...]
What is caveolar endocytosis? Caveolar endocytosis is a clathrin-independent endocytic process which involves bulb-shaped, 50-60nm plasma membrane invaginations called caveolae (or ‘little caves’). Caveolae formation is driven by integral membrane proteins called caveolins as well as peripheral membrane proteins called cavins (reviewed in [1]). [...]
What is clathrin-mediated endocytosis? Clathrin-mediated endocytosis (CME) is a vesicular transport event that facilitates the internalization and recycling of receptors engaged in a variety of processes, including signal transduction (G-protein and tyrosine kinase receptors), nutrient uptake and synaptic vesicle reformation [1]. Two classical examples [...]
How is clathrin recruited to the plasma membrane? Clathrin-mediated endocytosis is triggered by phosphatidylinositol-4,5-bisphosphate (PIP2) accumulation within the plasma membrane. PIP2 accumulates as a result of phosphoinositide catalysis by the lipid kinases, phosphatidylinositol-4-kinase (PI4K) and phosphatidylinositol-4-phosphate-5-kinase (PI4P5K) [1], [2] and hydrolysis by phosphatases. The [...]
How does the clathrin coated pit form? Adaptor proteins such as AP-2, AP180 and CALM (Clathrin-assembly lymphoid myeloid leukaemia protein), which accumulate within the lipid bilayer, are responsible for the recruitment of the triskelion shaped Clathrin trimer. This trimer does not interact with the [...]
How does scission of the clathrin-coated vesicle occur? As mentioned, in mammalian CME the GTPase dynamin is believed to play important roles in invagination and clathrin-coated pit (CCP) maturation [1]. Its binding partners endophilin and amphiphysin, can also induce tubulation of the vesicles and [...]
How are clathrin-coated vesicles uncoated? Uncoating is the process by which clathrin is removed from clathrin-coated vesicles (CCVs). In mammals, this ATP dependent process is driven by the 70kDa molecular chaperone ‘Heat shock cognate protein’. Although the exact mechanics of clathrin disassembly remain unclear, [...]
How are clathrin-coated vesicles transported? Different cytoskeletal networks have been implicated in the transport of clathrin-coated vesicles (CCVs). In yeast, the actin cytoskeleton traffics dissociated CCVs [1], whilst in mammals the microtubule network transports is involved in the sorting of CCVs to distinct populations [...]
What is the CLIC/GEEC Endocytosis pathway? The CLIC/GEEC (CG) pathway is a clathrin-independent endocytic pathway mediated by uncoated tubulovesicular primary carriers called clathrin-independent carriers (CLICs) which arise directly from the plasma membrane and later mature into tubular early endocytic compartments called Glycosylphosphotidylinositol- anchored protein [...]
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One of four Research Centres of Excellence at NUS, MBI is working to identify, measure and describe how the forces for motility and morphogenesis are expressed at the molecular, cellular and tissue level.