Maturation models for endosome and lysosome biogenesis

Core Protein Machinery for Mammalian Phosphatidylinositol 3,5-Bisphosphate Synthesis and Turnover That Regulates the Progression of Endosomal Transport

“…Fractions were monitored for 3 H and 32 P radioactivity by an on-line flow scintillation analyzer. 32 P radioactivity was plotted, and the counts within the elution times corresponding to the [ 32 P]GroPIns peaks determined by the above 3 H/ 32 P-labeled standards were summed (total PI radioactivity). The [ 32 P]PtdIns(3,5)P 2 and [ 32 P]PtdIns(3)P were then calculated as a percentage of total PI radioactivity and expressed relatively to the PtdIns(3)P or PtdIns(3,5)P 2 values of the control in each experiment (mean Ϯ S.E., four independent experiments).…”

“…[ 32 P]PtdIns(3,4)P 2 that were synthesized with PIKfyve and PI 3-kinase as described previously (14,38,43). FLO-ONE radiochromatography software (Packard Instrument Co.) was used for data evaluation.…”

“…According to the vesicle-transport model, endosome carrier vesicles (ECV) or multivesicular bodies (MVBs) arise by budding/detachment from early endosomes (23, 28 -30). An alternative model views early endosome maturation as a means of cargo transport (31)(32)(33). A recent study appears to reconcile both models by adapting elements of each one (34).…”

Endocytosis and vesicular trafficking of immune complexes and activation of phospholipase D by the human high-affinity IgG receptor requires distinct phosphoinositide 3-kinase activities

“…These destinations include a putative recycling compartment, the transGolgi network, and from these destinations they can subsequently be diverted to a lysosomal degradative\storage compartment [24]. The mechanisms underlying the passage of ligands from early endosomes through deep-lying, late endosomes on the way to lysosome degradation is controversial as to whether it results from vesicular trafficking or endosome maturation [25,26]. The vacuolar structures observed following FcγRI aggregation are similar to those observed in newborn-rat kidney cells in which wortmannin was used to block traffic out of the endosomal system [27], and it is likely that these structures represent swollen late-endosomal compartments, suggesting that these late-endosomal compartments become saturated and consequently swollen following FcγRI-internalized immune complexes.…”

Degradation of yolk platelets in the early amphibian embryo is regulated by fusion with late endosomes

“…Mastoparan activates GTP-binding regulatory proteins (G proteins;Higashijima et al 1988;Kikkawa et al 1992;Klinker et al 1996), which play important roles in the endocytic pathway (Olkkonen & Stenmark 1997). Pepstatin A has the ability to bind with cathepsin specifically (Matthews et al 1981), and it has been shown to inhibit fusion of endosomes with yolk platelets during amphibian oogenesis (Opresko & Karpf 1987 (Fagotto et al 1994b (Maxfield 1985;Mellman et al 1986;Murphy 1991 (Fagotto & Maxfield 1994a (Barinaga 1993;Sollner et al 1993;Ferro-Novick & Jahn 1994), which has been proposed to explain the secretion of synaptic vesicles in neurons, may also operate in the processes involved in the docking and fusion of the late endosome with the yolk membrane. Recent studies have shown that the mechanism described in the SNARE hypothesis plays important roles in intracellular transport in epithelial cells (Weimbs et al 1997).…”