2018
DOI: 10.1038/s41564-018-0167-x
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Abstract: LC3-associated phagocytosis (LAP) is a non-canonical autophagy pathway regulated by Rubicon, with an emerging role in immune homeostasis and antifungal host defence. Aspergillus cell wall melanin protects conidia (spores) from killing by phagocytes and promotes pathogenicity through blocking nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent activation of LAP. However, the signalling regulating LAP upstream of Rubicon and the mechanism of melanin-induced inhibition of this pathway remain inc… Show more

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Cited by 64 publications
(78 citation statements)
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“…Although the molecular mechanisms responsible for the activation of Rubicon and LAP are unclear, a recent study discovered that phagosomal calcium “leak” and that activation of calmodulin occurs upstream of Rubicon recruitment to the phagosome. The availability of phagosomal calcium is under the influence of melanin that can act to sequester the divalent cation thereby limiting calmodulin activation (Kyrmizi et al, ).…”
Section: Host Membranesmentioning
confidence: 99%
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“…Although the molecular mechanisms responsible for the activation of Rubicon and LAP are unclear, a recent study discovered that phagosomal calcium “leak” and that activation of calmodulin occurs upstream of Rubicon recruitment to the phagosome. The availability of phagosomal calcium is under the influence of melanin that can act to sequester the divalent cation thereby limiting calmodulin activation (Kyrmizi et al, ).…”
Section: Host Membranesmentioning
confidence: 99%
“…Although the molecular mechanisms responsible for the activation of Rubicon and LAP are unclear, a recent study discovered that phagosomal calcium "leak" and that activation of calmodulin occurs upstream of Rubicon recruitment to the phagosome. The availability of phagosomal calcium is under the influence of melanin that can act to sequester the divalent cation thereby limiting calmodulin activation (Kyrmizi et al, 2018). During infection, C. albicans undergoes a yeast-to-hyphae transition as a response to environmental stimuli including contact with host cells, nutrient deprivation, and increased pH (Jacobsen et al, 2012;Sudbery, 2011).…”
Section: Autophagy and Lc3-associated Phagocytosismentioning
confidence: 99%
“…This is best characterized in 10 phagocytic cells where LC3 associated phagocytosis (LAP) is activated by Toll-like receptor signaling resulting in recruitment of autophagy marker protein LC3 to the phagosome membrane to enhance phagosome maturation [1][2][3][4][5] . In non-phagocytes a similar non-canonical pathway recruits LC3 to endo-lysosome compartments during the uptake of particulate material such as apoptotic cells and aggregated β-amyloid and 15 following membrane damage during pathogen entry or osmotic imbalance induced by lysosomotropic drugs 6,7 8-10 . LC3 can be recruited to endo-lysosome compartments during the uptake of pathogens and extracellular material, but the roles played by noncanonical autophagy during infection in vivo are largely unknown.…”
Section: Discussionmentioning
confidence: 99%
“…At present a role for non-canonical autophagy in host defence has been implied from in vitro studies of LAP in phagocytes and microbes with a tropism for macrophages such as Listeria monocytogenes 11 , Legionella dumoffii 12 , Leishmania major and Aspergillus fumigatus [13][14][15] . Critically, these studies have rarely been extended to model organisms with intact epithelial barriers and complex immune systems.…”
Section: Discussionmentioning
confidence: 99%
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