Relevant bibliographies by topics / Endocytic maturation

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Academic literature on the topic 'Endocytic maturation'

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Published: 1 April 2023

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Journal articles on the topic "Endocytic maturation"

Thilo, L., E. Stroud, and T. Haylett. "Maturation of early endosomes and vesicular traffic to lysosomes in relation to membrane recycling." Journal of Cell Science 108, no. 4 (April 1, 1995): 1791–803. http://dx.doi.org/10.1242/jcs.108.4.1791.

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The controversy whether endocytic processing occurs by organellar maturation or by vesicular traffic has not been resolved. It is also not clear whether maturation continues to the stage of lysosomes, to what extent it involves a decrease in organellar fusogenicity, and how it relates to membrane recycling. Maturation and vesicular traffic imply distinct kinetics for the intermingling of endocytic markers after sequential endocytic uptake. We have studied the kinetics of intermingling of fluid-phase markers (fluorescein-labelled dextran and horseradish peroxidase) and cell surface-derived membrane (labelled by galactosylation) in organelles at early and late stages of the endocytic pathway in macrophage-like P388D1 cells. Intermingling declined by sigmoid kinetics, indicating that endosomes matured within about 3 minutes to become non-fusogenic towards early endosomes. During maturation about 60% of internalized membrane was recycled with T1/2 approximately 2 minutes. Whereas matured endosomes were non-fusogenic towards early endosomes and towards each other, a second phase of intermingling was observed upon delivery to lysosomes. This intermingling occurred by a first-order process (T1/2 approximately 4 minutes), concurrent with recycling of the remaining 40% of internalized membrane marker. These kinetic observations suggest a model for endocytic processing which reconciles maturation of early endosomes with the known function of carrier vesicles: Endocytic carrier vesicles do not bud off from permanent early endosomes as proposed for vesicular traffic, but are derived, together with recycling vesicles, from the maturation of early endosomes which are consumed by this process; these carrier vesicles subsequently mediate delivery to lysosomes by vesicular traffic during which the remaining surface-derived membrane is recycled.

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Carroll, Susheela Y., Helen E. M. Stimpson, Jasper Weinberg, Christopher P. Toret, Yidi Sun, and David G. Drubin. "Analysis of yeast endocytic site formation and maturation through a regulatory transition point." Molecular Biology of the Cell 23, no. 4 (February 15, 2012): 657–68. http://dx.doi.org/10.1091/mbc.e11-02-0108.

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The earliest stages of endocytic site formation and the regulation of endocytic site maturation are not well understood. Here we analyzed the order in which the earliest proteins are detectable at endocytic sites in budding yeast and found that an uncharacterized protein, Pal1p/Ydr348cp, is also present at the initial stages of endocytosis. Because Ede1p (homologue of Eps15) and clathrin are the early-arriving proteins most important for cargo uptake, their roles during the early stages of endocytosis were examined more comprehensively. Ede1p is necessary for efficient recruitment of most early-arriving proteins, but not for the recruitment of the adaptor protein Yap1802p, to endocytic sites. The early-arriving proteins, as well as the later-arriving proteins Sla2p and Ent1/2p (homologues of Hip1R and epsins), were found to have longer lifetimes in CLC1-knockout yeast, which indicates that clathrin light chain facilitates the transition from the intermediate to late coat stages. Cargo also arrives during the early stages of endocytosis, and therefore its effect on endocytic machinery dynamics was investigated. Our results are consistent with a role for cargo in regulating the transition of endocytic sites from the early stages of formation to the late stages during which vesicle formation occurs.

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Lu, Rebecca, and David G. Drubin. "Selection and stabilization of endocytic sites by Ede1, a yeast functional homologue of human Eps15." Molecular Biology of the Cell 28, no. 5 (March 2017): 567–75. http://dx.doi.org/10.1091/mbc.e16-06-0391.

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During clathrin-mediated endocytosis (CME), endocytic-site maturation can be divided into two stages corresponding to the arrival of the early and late proteins at the plasma membrane. The early proteins are required to capture cargo and position the late machinery, which includes proteins involved in actin assembly and membrane scission. However, the mechanism by which early-arriving proteins select and stabilize endocytic sites is not known. Ede1, one of the earliest proteins recruited to endocytic sites, facilitates site initiation and stabilization. Deletion of EDE1 results in fewer CME initiations and defects in the timing of vesicle maturation. Here we made truncation mutants of Ede1 to better understand how different domains contribute to its recruitment to CME sites, site selection, and site maturation. We found that the minimal domains required for efficient Ede1 localization at CME sites are the third EH domain, the proline-rich region, and the coiled-coil region. We also found that many strains expressing ede1 truncations could support a normal rate of site initiation but still had defects in site-maturation timing, indicating separation of Ede1 functions. When expressed in yeast, human Eps15 localized to the plasma membrane, where it recruited late-phase CME proteins and supported productive endocytosis, identifying it as an Ede1 functional homologue.

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Liu, Guojun, Paulomi Sanghavi, Kathryn E. Bollinger, Libby Perry, Brendan Marshall, Penny Roon, Tsubasa Tanaka, Akira Nakamura, and Graydon B. Gonsalvez. "Efficient Endocytic Uptake and Maturation inDrosophilaOocytes Requires Dynamitin/p50." Genetics 201, no. 2 (August 10, 2015): 631–49. http://dx.doi.org/10.1534/genetics.115.180018.

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Stevens-Hernandez, Christian J., and Lesley J. Bruce. "Reticulocyte Maturation." Membranes 12, no. 3 (March 10, 2022): 311. http://dx.doi.org/10.3390/membranes12030311.

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Changes to the membrane proteins and rearrangement of the cytoskeleton must occur for a reticulocyte to mature into a red blood cell (RBC). Different mechanisms of reticulocyte maturation have been proposed to reduce the size and volume of the reticulocyte plasma membrane and to eliminate residual organelles. Lysosomal protein degradation, exosome release, autophagy and the extrusion of large autophagic–endocytic hybrid vesicles have been shown to contribute to reticulocyte maturation. These processes may occur simultaneously or perhaps sequentially. Reticulocyte maturation is incompletely understood and requires further investigation. RBCs with membrane defects or cation leak disorders caused by genetic variants offer an insight into reticulocyte maturation as they present characteristics of incomplete maturation. In this review, we compare the structure of the mature RBC membrane with that of the reticulocyte. We discuss the mechanisms of reticulocyte maturation with a focus on incomplete reticulocyte maturation in red cell variants.

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Dumas, Audrey, Gabrielle Lê-Bury, Florence Marie-Anaïs, Floriane Herit, Julie Mazzolini, Thomas Guilbert, Pierre Bourdoncle, et al. "The HIV-1 protein Vpr impairs phagosome maturation by controlling microtubule-dependent trafficking." Journal of Cell Biology 211, no. 2 (October 26, 2015): 359–72. http://dx.doi.org/10.1083/jcb.201503124.

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Human immunodeficiency virus type 1 (HIV-1) impairs major functions of macrophages but the molecular basis for this defect remains poorly characterized. Here, we show that macrophages infected with HIV-1 were unable to respond efficiently to phagocytic triggers and to clear bacteria. The maturation of phagosomes, defined by the presence of late endocytic markers, hydrolases, and reactive oxygen species, was perturbed in HIV-1–infected macrophages. We showed that maturation arrest occurred at the level of the EHD3/MICAL-L1 endosomal sorting machinery. Unexpectedly, we found that the regulatory viral protein (Vpr) was crucial to perturb phagosome maturation. Our data reveal that Vpr interacted with EB1, p150Glued, and dynein heavy chain and was sufficient to critically alter the microtubule plus end localization of EB1 and p150Glued, hence altering the centripetal movement of phagosomes and their maturation. Thus, we identify Vpr as a modulator of the microtubule-dependent endocytic trafficking in HIV-1–infected macrophages, leading to strong alterations in phagolysosome biogenesis.

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Lennon-Duménil, Ana-Maria, Arnold H. Bakker, René Maehr, Edda Fiebiger, Herman S. Overkleeft, Mario Rosemblatt, Hidde L. Ploegh, and Cécile Lagaudrière-Gesbert. "Analysis of Protease Activity in Live Antigen-presenting Cells Shows Regulation of the Phagosomal Proteolytic Contents During Dendritic Cell Activation." Journal of Experimental Medicine 196, no. 4 (August 19, 2002): 529–40. http://dx.doi.org/10.1084/jem.20020327.

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Here, we describe a new approach designed to monitor the proteolytic activity of maturing phagosomes in live antigen-presenting cells. We find that an ingested particle sequentially encounters distinct protease activities during phagosomal maturation. Incorporation of active proteases into the phagosome of the macrophage cell line J774 indicates that phagosome maturation involves progressive fusion with early and late endocytic compartments. In contrast, phagosome biogenesis in bone marrow–derived dendritic cells (DCs) and macrophages preferentially involves endocytic compartments enriched in cathepsin S. Kinetics of phagosomal maturation is faster in macrophages than in DCs. Furthermore, the delivery of active proteases to the phagosome is significantly reduced after the activation of DCs with lipopolysaccharide. This observation is in agreement with the notion that DCs prevent the premature destruction of antigenic determinants to optimize T cell activation. Phagosomal maturation is therefore a tightly regulated process that varies according to the type and differentiation stage of the phagocyte.

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Mettlen, Marcel, Ping-Hung Chen, Saipraveen Srinivasan, Gaudenz Danuser, and Sandra L. Schmid. "Regulation of Clathrin-Mediated Endocytosis." Annual Review of Biochemistry 87, no. 1 (June 20, 2018): 871–96. http://dx.doi.org/10.1146/annurev-biochem-062917-012644.

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Clathrin-mediated endocytosis (CME) is the major endocytic pathway in mammalian cells. It is responsible for the uptake of transmembrane receptors and transporters, for remodeling plasma membrane composition in response to environmental changes, and for regulating cell surface signaling. CME occurs via the assembly and maturation of clathrin-coated pits that concentrate cargo as they invaginate and pinch off to form clathrin-coated vesicles. In addition to the major coat proteins, clathrin triskelia and adaptor protein complexes, CME requires a myriad of endocytic accessory proteins and phosphatidylinositol lipids. CME is regulated at multiple steps—initiation, cargo selection, maturation, and fission—and is monitored by an endocytic checkpoint that induces disassembly of defective pits. Regulation occurs via posttranslational modifications, allosteric conformational changes, and isoform and splice-variant differences among components of the CME machinery, including the GTPase dynamin. This review summarizes recent findings on the regulation of CME and the evolution of this complex process.

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Sturgill-Koszycki, Sheila, and Michele S. Swanson. "Legionella pneumophila Replication Vacuoles Mature into Acidic, Endocytic Organelles." Journal of Experimental Medicine 192, no. 9 (October 30, 2000): 1261–72. http://dx.doi.org/10.1084/jem.192.9.1261.

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After ingestion by macrophages, Legionella pneumophila inhibits acidification and maturation of its phagosome. After a 6–10-h lag period, the bacteria replicate for 10–14 h until macrophage lysis releases dozens of progeny. To examine whether the growth phase of intracellular L. pneumophila determines the fate of its phagosome, interactions between the endosomal network and pathogen vacuoles were analyzed throughout the primary infection period. Surprisingly, as L. pneumophila replicated exponentially, a significant proportion of the vacuoles acquired lysosomal characteristics. By 18 h, 70% contained lysosomal-associated membrane protein 1 (LAMP-1) and 40% contained cathepsin D; 50% of the vacuoles could be labeled by endocytosis, and the pH of this population of vacuoles averaged 5.6. Moreover, L. pneumophila appeared to survive and replicate within lysosomal compartments: vacuoles harboring more than five bacteria also contained LAMP-1, inhibition of vacuole acidification and maturation by bafilomycin A1 inhibited bacterial replication, bacteria within endosomal vacuoles responded to a metabolic inducer by expressing a gfp reporter gene, and replicating bacteria obtained from macrophages, but not broth, were acid resistant. Understanding how L. pneumophila first evades and then exploits the endosomal pathway to replicate within macrophages may reveal the mechanisms governing phagosome maturation, a process also manipulated by Mycobacteria, Leishmania, and Coxiella.

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Merrill, Nathan M., Joshua L. Schipper, Jonathan B. Karnes, Audra L. Kauffman, Katie R. Martin, and Jeffrey P. MacKeigan. "PI3K-C2α knockdown decreases autophagy and maturation of endocytic vesicles." PLOS ONE 12, no. 9 (September 14, 2017): e0184909. http://dx.doi.org/10.1371/journal.pone.0184909.

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Dissertations / Theses on the topic "Endocytic maturation"

Archer, Madeline A., Teal M. Brechtel, Leslie E. Davis, Rinkuben C. Parmar, Mohammad H. Hasan, and Ritesh Tandon. "Inhibition of endocytic pathways impacts cytomegalovirus maturation." NATURE PUBLISHING GROUP, 2017. http://hdl.handle.net/10150/623928.

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Endocytic processes are critical for cellular entry of several viruses; however, the role of endocytosis in cellular trafficking of viruses beyond virus entry is only partially understood. Here, we utilized two laboratory strains (AD169 and Towne) of human cytomegalovirus (HCMV), which are known to use cell membrane fusion rather than endocytosis to enter fibroblasts, in order to study a post-entry role of endocytosis in HCMV life cycle. Upon pharmacological inhibition of dynamin-2 or clathrin terminal domain (TD) ligand association, these strains entered the cells successfully based on the expression of immediate early viral protein. However, both the inhibitors significantly reduced the growth rates and final virus yields of viruses without inhibiting the expression of early to late viral proteins. Clathrin accumulated in the cytoplasmic virus assembly compartment (vAC) of infected cells co-localizing with virus tegument protein pp150 and the formation of vAC was compromised upon endocytic inhibition. Transmission electron micrographs (TEM) of infected cells treated with endocytosis inhibitors showed intact nuclear stages of nucleocapsid assembly but the cytoplasmic virus maturation was greatly compromised. Thus, the data presented here implicate endocytic pathways in HCMV maturation and egress.

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Shah, Ankur H. "Adenovirus RIDalpha Regulates Endosome Maturation by Mimicking GTP-Rab7." Case Western Reserve University School of Graduate Studies / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=case1181051279.

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Dumas, Audrey. "Macrophage et infection par le VIH‐1 : perturbation des fonctions de clairance et d’activation." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T039/document.

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La phagocytose, fonction fondamentale des macrophages, est un processus qui se décompose en deux étapes bien distinctes : les étapes précoces d’internalisation menant à la formation du phagosome et les étapes tardives de maturation du phagosome. Le virus de l’immunodéficience humaine de type I (VIH-1) infecte les macrophages, ce qui perturbe leurs fonctions. L’effet de l’infection virale dans ces cellules est peu caractérisé en comparaison des lymphocytes T. Des travaux antérieurs ont montré d’une part que l’étape précoce d’internalisation de larges particules et bactéries était bloquée de moitié dans les macrophages primaires humains infectés par le VIH-1 via Nef, la protéine de virulence majeure du virus et d’autres part, que la réponse cytokinique était atténuée chez les patients infectés. Ainsi, nous avons étudié l’effet du VIH-1 sur les étapes tardives de la phagocytose : la maturation du phagosome et l’activation des macrophages qui en résulte. Nous avons montré que le VIH-1 altère les étapes tardives de la phagocytose en inhibant la maturation du phagosome, définie par le recrutement de marqueurs tardifs de la voie d’endocytose, d’hydrolases et la production d’espèces réactives oxygénées. Malgré une pré-activation basale, les macrophages infectés par le VIH-1 sont incapables de répondre efficacement à une stimulation induite par phagocytose, ce qui conduit à une modulation de la réponse transcriptionnelle et cytokinique. La dynamique des microtubules et la migration centripète des phagosomes sont profondément affectées par le virus. De façon inattendue, la protéine virale Vpr est impliquée dans ces perturbations, alors que Nef ne joue pas de rôle notable. Nos résultats indiquent que les composants intracellulaires de la machinerie de tri endosomal sont détournés par le compartiment viral dans les macrophages infectés. Par cette étude, nous avons donc identifié la protéine Vpr comme nouveau modulateur de la dynamique des microtubules et du trafic intracellulaire, entraînant ainsi une altération profonde de la maturation du phagosome et de la clairance bactérienne dans les macrophages infectés. Ce travail contribue à mieux comprendre l’établissement d’infections opportunistes chez les patients infectés
Phagocytosis, a crucial function of macrophages, is composed of two well defined steps : the early step of internalization leading to phagosome formation and the late step of phagosome maturation. The immunodeficiency virus type I (HIV-1) infects macrophages, which disturbs theirs functions. The effects of HIV-1 infection are poorly characterized in this cell type compared to T lymphocytes. Previous results have already shown that the early step of internalization of large particles and bacteria are half blocked by Nef in HIV-1 infected primary macrophages and that the cytokine response is attenuated in infected patients. Thus, we have studied the effect of HIV-1 infection on the late step of phagocytosis : phagosome maturation and the resulting macrophage activation. We shown that HIV-1 impairs late phagocytic events affecting the phagosome maturation, as defined by late endocytic markers and hydrolases recruitment, and reactives oxygens species production. HIV-1 infected macrophages exhibited a basal preactivation but appeared unable to respond efficiently to phagocytic triggers leading to cytokine and transcriptional modifications. Centripetal migration of phagosomes and microtubule dynamics were deeply altered upon viral infection. Surprisingly, the Vpr viral protein was implicated in these pertubations, while Nef was not. Our results revealed that elements of the endosomal sorting machinery were hijacked to the virus-containing compartments in HIV-infected macrophages. With this study, we identify Vpr as a modulator of the microtubule dynamics and intracellular trafficking, leading to alterations in phagosome maturation and bacterial clearance in HIV-1 infected macrophages. This work contribute to better understanding of the establishment of opportunistic infections in HIV-infected patients

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Shetty, Aparna [Verfasser]. "The neural cell adhesion molecule NCAM promotes maturation of the presynaptic endocytic machinery by switching synaptic vesicle recycling from AP3- to AP2-dependent mechanism in mice (Mus musculus, strain C57Bl/6J). / by Aparna Shetty." 2008. http://d-nb.info/989006360/34.

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Book chapters on the topic "Endocytic maturation"

Wallace, R. A., Lee Opresko, H. S. Wiley, and Kelly Selman. "The Oocyte as an Endocytic Cell." In Ciba Foundation Symposium 98 - Molecular Biology of Egg Maturation, 228–48. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470720790.ch13.

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Benarroch, Eduardo E. "Vesicular Trafficking." In Neuroscience for Clinicians, edited by Eduardo E. Benarroch, 106–25. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780190948894.003.0007.

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Normal cell function depends on the appropriate synthesis, maturation, sorting, and delivery of fully processed proteins and other macromolecules to specific intracellular compartments; uptake of material from the cell exterior; and regulated intracellular processing and degradation of proteins, lipids, complex carbohydrates, abnormal aggregates, and senescent organelles. These fundamental functions involve secretory, endocytic, and autophagic pathways. The secretory pathway is responsible for protein maturation, sorting, and delivery of transmembrane and secreted proteins from their site of synthesis to their final destinations. Synaptic vesicle exocytosis is a special form of secretion that allows rapid communication between neurons. The endocytic pathway starts with the internalization of material via endosomes. Endosomal content can be transported back to the cell body, recycled to cell compartments, or delivered for degradation by the lysosome. Abnormal protein aggregates or damaged organelles undergo autophagy, which involves formation of an autophagosome and degradation by the lysosome. Impaired vesicular trafficking is a fundamental mechanism in a large number of neurodegenerative disorders, including hereditary spastic paraplegia, lower motor neuron syndromes, and Parkinson disease.

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