Powering membrane traffic in endocytosis and recycling

Abstract

| Early in evolution, the diversification of membrane-bound compartments that characterize eukaryotic cells was accompanied by the elaboration of molecular machineries that mediate intercompartmental communication and deliver materials to specific destinations. Molecular motors that move on tracks of actin filaments or microtubules mediate the movement of organelles and transport between compartments. The subjects of this review are the motors that power the transport steps along the endocytic and recycling pathways, their modes of attachment to cargo and their regulation.The emergence of eukaryotic cells was accompanied by the development of endomembrane systems that compartmentalize biochemical pathways and biosynthetic processes. An evolutionary trend towards increasing complexity and subcellular specialization necessitated the development of machineries for intercompartmental communication. Molecular assemblies evolved to confer specificity to the interactions of donor and acceptor compartments (budding, sorting, tethering and fusion). Cytoskeletal polymers such as actin filaments and microtubules, which help segregate genetic material and determine cell shape and subcellular architecture, were co-opted as tracks for transport. In animal cells, microtubules support long-range transport, whereas the more flexible actin filaments serve short-range movements both near the cell periphery and in the cell interior. Also, actin filaments can be woven into dense networks of short fibres through the action of crosslinkers and branchpromoting complexes. On the other hand, in many plant cells, bundled actin filaments can form extended tracks for long-distance transport. Owing to the gel-like nature of the cytoplasm, the Brownian movement of organelles is severely restricted and cargoes have to be transported to their destinations at the expense of energy. Furthermore, seemingly random, but motor-dependent, movement is proposed to increase the probability of vesicle collisions and therefore promote fusion events. Movement is powered by three ATP-dependent motors: myosin, kinesin and dynein. Over the course of eukaryotic evolution, these motors have diversified into a large number of families with specific tasks (FIG. 1).Here, we review the involvement of molecular motors in the movement of endosomes and in vesicular trafficking along the endocytic and recycling pathways. These pathways are summarized in FIG. 2. We do not, however,

Endoplasmic Reticulum Chaperone Protein GRP-78 Mediates Endocytosis of Dentin Matrix Protein 1

“…Endocytic vesicles are normally transported either through microfilaments or via the microtubules. Microfilaments are used for short range transport, and the microtubules are used for long range transport (28). Results in Fig.…”

α-Synuclein and Its A30P Mutant Affect Actin Cytoskeletal Structure and Dynamics

“…In the migration test, in fact, the A30P ␣-synuclein-rich cells were almost immobile; the constitutive membrane traffic to and from the plasma membrane was larger in both MDCK and N2A cells; however, the responses to ATP and high K ϩ stimulation were completely ineffective or only weak, respectively. The membrane traffic results could be related to the disruption in the A30P ␣-synuclein-expressing cells of the actin barrier below the plasma membrane (Soldati and Schliwa, 2006). This structure, in fact, appears to decrease the probability of spontaneous vesicle exocytosis in resting cells.…”

Delivery of chemotherapeutic drugs in tumour cell-derived microparticles

“…To better understand drug-packaging MP-mediated tumour cell killing, the mechanism involved in tumour cell release and uptake of MPs was investigated. The cytoskeleton has important roles in cellular endocytosis and exocytosis [23][24][25][26] , leading to the possible requirement of cytoskeletal proteins for the release and uptake of MPs by tumour cells. When H22 cells were treated with cytochalasin D, an inhibitor of F-actin polymerization, actin filament formation was inhibited, resulting in decreased MP release, induced by ultraviolet irradiation (Fig.…”