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Comptes Rendus Biologies Jun 2012Large numbers of publications investigating the molecular details, the regulation and the physiological roles of autophagic processes have appeared over the last few... (Review)
Review
Large numbers of publications investigating the molecular details, the regulation and the physiological roles of autophagic processes have appeared over the last few years, dealing with animals, plants and unicellular eukaryotic organisms. This strong interest is caused by the fact that autophagic processes are ubiquitous in eukaryotic organisms. They are involved in the adaptation of organisms to their environment and to stressful conditions, thereby contributing to cell and organism survival and longevity. This review article aims to describe the discovery of autophagy, the molecular details of this complex process, its regulation, and its specific functions in plants.
Topics: Adaptation, Physiological; Arabidopsis Proteins; Autophagy; Botany; Chloroplasts; Energy Metabolism; Genes, Plant; Intracellular Membranes; Models, Biological; Phagosomes; Plant Cells; Plant Physiological Phenomena; Plants; Vacuoles
PubMed: 22721559
DOI: 10.1016/j.crvi.2012.04.004 -
Microbiology and Immunology Jul 2011Autophagy is the host innate immune system's first line of defense against microbial intruders. When the innate defense system recognizes invading bacterial pathogens... (Review)
Review
Autophagy is the host innate immune system's first line of defense against microbial intruders. When the innate defense system recognizes invading bacterial pathogens and their infection processes, autophagic proteins act as cytosolic sensors that allow the autophagic pathway to be rapidly activated. However, many intracellular bacterial pathogens deploy highly evolved mechanisms to evade autophagic recognition, manipulate the autophagic pathway, and remodel the autophagosomal compartment for their own benefit. Here current topics regarding the recognition of invasive bacteria by the cytosolic innate immune system are highlighted, including autophagy and the mechanisms that enable bacteria to evade autophagy. Also highlighted are some selective examples of bacterial activities that manipulate the autophagic pathways for their own benefit.
Topics: Autophagy; Bacteria; Humans; Immune Evasion; Immunity, Innate; Models, Biological; Phagosomes
PubMed: 21707736
DOI: 10.1111/j.1348-0421.2011.00343.x -
Nature Reviews. Microbiology Apr 2004Intracellular bacteria and viruses must survive the vigorous antimicrobial responses of their hosts to replicate successfully. The cellular process of autophagy — in... (Review)
Review
Intracellular bacteria and viruses must survive the vigorous antimicrobial responses of their hosts to replicate successfully. The cellular process of autophagy — in which compartments bound by double membranes engulf portions of the cytosol and then mature to degrade their cytoplasmic contents — is likely to be one such host-cell response. Several lines of evidence show that both bacteria and viruses are vulnerable to autophagic destruction and that successful pathogens have evolved strategies to avoid autophagy, or to actively subvert its components, to promote their own replication. The molecular mechanisms of the avoidance and subversion of autophagy by microorganisms will be the subject of much future research, not only to study their roles in the replication of these microorganisms, but also because they will provide — as bacteria and viruses so often have — unique tools to study the cellular process itself.
Topics: Animals; Autophagy; Bacterial Physiological Phenomena; Humans; Phagosomes; Signal Transduction; Virus Physiological Phenomena
PubMed: 15031729
DOI: 10.1038/nrmicro865 -
International Journal of Molecular... Mar 2020Autophagy is an evolutionarily conserved process that occurs in yeast, plants, and animals. Despite many years of research, some aspects of autophagy are still not fully... (Review)
Review
Autophagy is an evolutionarily conserved process that occurs in yeast, plants, and animals. Despite many years of research, some aspects of autophagy are still not fully explained. This mostly concerns the final stages of autophagy, which have not received as much interest from the scientific community as the initial stages of this process. The final stages of autophagy that we take into consideration in this review include the formation and degradation of the autophagic bodies as well as the efflux of metabolites from the vacuole to the cytoplasm. The autophagic bodies are formed through the fusion of an autophagosome and vacuole during macroautophagy and by vacuolar membrane invagination or protrusion during microautophagy. Then they are rapidly degraded by vacuolar lytic enzymes, and products of the degradation are reused. In this paper, we summarize the available information on the trafficking of the autophagosome towards the vacuole, the fusion of the autophagosome with the vacuole, the formation and decomposition of autophagic bodies inside the vacuole, and the efflux of metabolites to the cytoplasm. Special attention is given to the formation and degradation of autophagic bodies and metabolite salvage in plant cells.
Topics: Autophagosomes; Autophagy; Biological Transport; Cytoplasm; Phagosomes; Plant Physiological Phenomena; Proteolysis; Vacuoles
PubMed: 32210003
DOI: 10.3390/ijms21062205 -
Current Biology : CB Feb 2023Cutting up food into small pieces is well known to improve digestion. New work now shows that this concept also applies in the cellular world, by demonstrating that...
Cutting up food into small pieces is well known to improve digestion. New work now shows that this concept also applies in the cellular world, by demonstrating that phagolysosome vesiculation promotes cell corpse degradation in Caenorhabditis elegans blastomeres.
Topics: Animals; Phagocytosis; Phagosomes; Blastomeres; Cadaver; Caenorhabditis elegans
PubMed: 36854271
DOI: 10.1016/j.cub.2023.01.017 -
Science (New York, N.Y.) Nov 2004Autophagy, the process by which cells recycle cytoplasm and dispose of excess or defective organelles, has entered the research spotlight largely owing to the discovery... (Review)
Review
Autophagy, the process by which cells recycle cytoplasm and dispose of excess or defective organelles, has entered the research spotlight largely owing to the discovery of the protein components that drive this process. Identifying the autophagy genes in yeast and finding orthologs in other organisms reveals the conservation of the mechanism of autophagy in eukaryotes and allows the use of molecular genetics and biology in different model systems to study this process. By mostly morphological studies, autophagy has been linked to disease processes. Whether autophagy protects from or causes disease is unclear. Here, we summarize current knowledge about the role of autophagy in disease and health.
Topics: Animals; Apoptosis; Autophagy; Humans; Infections; Muscular Diseases; Neoplasms; Neurodegenerative Diseases; Phagosomes
PubMed: 15528435
DOI: 10.1126/science.1099993 -
Scientific Reports Jul 2017Erythrophagocytosis, the phagocytic removal of damaged red blood cells (RBC), and subsequent phagolysosome biogenesis are important processes in iron/heme metabolism and...
Erythrophagocytosis, the phagocytic removal of damaged red blood cells (RBC), and subsequent phagolysosome biogenesis are important processes in iron/heme metabolism and homeostasis. Phagolysosome biogenesis implies the interaction of nascent phagosomes with endocytic compartments and also autophagy effectors. Here, we report that besides recruitment of microtubule-associated protein-1-light chain 3 (LC3), additional autophagy machinery such as sequestosome 1 (p62) is also acquired by single-membrane phagosomes at very early stages of the phagocytic process and that its acquisition is very important to the outcome of the process. In bone marrow-derived macrophages (BMDM) silenced for p62, RBC degradation is inhibited. P62, is also required for nuclear translocation and activation of the transcription factor Nuclear factor E2-related Factor 2 (NRF2) during erythrophagocytosis. Deletion of the Nrf2 allele reduces p62 expression and compromises RBC degradation. In conclusion, we reveal that erythrophagocytosis relies on an interplay between p62 and NRF2, potentially acting as protective mechanism to maintain reactive oxygen species at basal levels and preserve macrophage homeostasis.
Topics: Animals; Autophagy; Cell Line; Erythrocytes; Gene Expression Regulation; Humans; Intracellular Space; Mice, Inbred C57BL; Mice, Knockout; Microtubule-Associated Proteins; NF-E2-Related Factor 2; Phagocytosis; Phagosomes; Phosphorylation; Rabbits; Sequestosome-1 Protein; Signal Transduction; Ubiquitin
PubMed: 28724916
DOI: 10.1038/s41598-017-05687-1 -
Traffic (Copenhagen, Denmark) Aug 2012Ancient protozoan phagocytes and modern professional phagocytes of metazoans, such as macrophages, employ evolutionarily conserved mechanisms to kill microbes. These... (Review)
Review
Ancient protozoan phagocytes and modern professional phagocytes of metazoans, such as macrophages, employ evolutionarily conserved mechanisms to kill microbes. These mechanisms rely on microbial ingestion, followed by maturation of the phagocytic vacuole, or so-called phagosome. Phagosome maturation includes a series of fusion and fission events with the host cell endosomes and lysosomes, leading to a rapid increase of the degradative properties of the vacuole and to the destruction of the ingested microbe within a very hostile intracellular compartment, the phagolysosome. Historically, the mechanisms and weapons used by phagocytes to kill microbes have been separated into different classes. Phagosomal acidification, together with the production of reactive oxygen and nitrogen species, the selective manipulation of various ions in the phagosomal lumen, and finally the engagement of a battery of acidic hydrolases, are well-recognized players in this process. However, it is relatively recently that interconnections among these mechanisms have become apparent. In this review, we will focus on some emerging concepts about these interconnected aspects of the warfare at the host-pathogen interface, using mostly Mycobacterium tuberculosis as an example of intracellular pathogen. In particular, recent discoveries on the role of phagosomal ions and other chemicals in the control of pathogens, as well as mechanisms evolved by intracellular pathogens to circumvent or even exploit the weapons of the host cell will be discussed.
Topics: Animals; Humans; Hydrogen-Ion Concentration; Hydrolases; Macrophages; Metals; Mycobacteriaceae; Mycobacterium tuberculosis; Phagocytosis; Phagosomes; Reactive Nitrogen Species; Reactive Oxygen Species; Respiratory Burst; Salts
PubMed: 22462580
DOI: 10.1111/j.1600-0854.2012.01358.x -
Toxicology and Applied Pharmacology Mar 2017NLRP3 inflammasome activation occurs in response to hazardous particle exposures and is critical for the development of particle-induced lung disease. Mechanisms of...
NLRP3 inflammasome activation occurs in response to hazardous particle exposures and is critical for the development of particle-induced lung disease. Mechanisms of Lysosome Membrane Permeabilization (LMP), a central pathway for activation of the NLRP3 inflammasome by inhaled particles, are not fully understood. We demonstrate that the lysosomal vATPases inhibitor Bafilomycin A1 blocked LMP in vitro and ex vivo in primary murine macrophages following exposure to silica, multi-walled carbon nanotubes, and titanium nanobelts. Bafilomycin A1 treatment of particle-exposed macrophages also resulted in decreased active cathepsin L in the cytosol, a surrogate measure for leaked cathepsin B, which was associated with less NLRP3 inflammasome activity. Silica-induced LMP was partially dependent upon lysosomal cathepsins B and L, whereas nanoparticle-induced LMP occurred independent of cathepsin activity. Furthermore, inhibition of lysosomal cathepsin activity with CA-074-Me decreased the release of High Mobility Group Box 1. Together, these data support the notion that lysosome acidification is a prerequisite for particle-induced LMP, and the resultant leak of lysosome cathepsins is a primary regulator of ongoing NLRP3 inflammasome activity and release of HMGB1.
Topics: Animals; Cell Membrane Permeability; Cells, Cultured; Chemical Engineering; Female; Inflammasomes; Intracellular Membranes; Lysosomes; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; NLR Family, Pyrin Domain-Containing 3 Protein; Nanoparticles; Phagosomes; Silicon Dioxide
PubMed: 28126413
DOI: 10.1016/j.taap.2017.01.012 -
Traffic (Copenhagen, Denmark) Apr 2007Phagosomes are fascinating subcellular structures. After all, there are only a few compartments that are born before our very eyes and whose development we can follow in... (Review)
Review
Phagosomes are fascinating subcellular structures. After all, there are only a few compartments that are born before our very eyes and whose development we can follow in a light microscope until their contents disintegrate and are completely absorbed. Yet, some phagosomes are taken advantage of by pathogenic microorganisms, which change their fate. Research into phagosome biogenesis has flourished in recent years - the purpose of this review is to give a glimpse of where this research stands, with emphasis on the cell biology of macrophage phagosomes, on new model organisms for the study of phagosome biogenesis and on intracellular pathogens and their interference with normal phagosome function.
Topics: Animals; Endosomes; Humans; Phagocytosis; Phagosomes; Vacuoles
PubMed: 17274798
DOI: 10.1111/j.1600-0854.2006.00531.x