Membrane tubulovesicular extensions (cytonemes)

Galkina, Svetlana I.; Федорова, Н. В.; Stadnichuk, Vladimir I.; Sud’ina, Galina F.

doi:10.4161/cam.23130

Cited by 14 publications

(8 citation statements)

References 127 publications

(208 reference statements)

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“…Formation cytonemes under the influence of actin-depolymerizing alkaloids may occur due to blockage of the separation of secretory vesicles from the plasma membrane and from each other [ 20 , 21 , 27 ]. As a result, secretory trafficking extends outward the cells as cytonemes, which consist of membrane vesicles and tubes of the same diameter lined up in a row.…”

Section: Discussionmentioning

confidence: 99%

“…We observed the formation of cytonemes in human neutrophils upon the inhibition of vacuolar-type ATPase, the blocking of glucose metabolism, the inhibition of GTPase dynamin, or in the presence of nitric oxide donor diethylamine NONOate or cytochalasin D [ 18 , 21 , 22 , 25 – 27 ]. Proteome analysis has revealed that (i) the cytonemes contain bactericides of primary and secondary secretory granules, cytoplasmic proteins such as actin cytoskeleton and S100 proteins, and energy-metabolizing (presumably glycolytic) enzymes and (ii) the content of cytonemes does not depend on agent inducing their formation [ 20 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

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Mold Alkaloid Cytochalasin D Modifies the Morphology and Secretion of fMLP-, LPS-, or PMA-Stimulated Neutrophils upon Adhesion to Fibronectin

Galkina

Федорова

Serebryakova

et al. 2017

Mediators of Inflammation

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Neutrophils play an essential role in innate immunity due to their ability to migrate into infected tissues and kill microbes with bactericides located in their secretory granules. Neutrophil transmigration and degranulation are tightly regulated by actin cytoskeleton. Invading pathogens produce alkaloids that cause the depolymerization of actin, such as the mold alkaloid cytochalasin D. We studied the effect of cytochalasin D on the morphology and secretion of fMLP-, LPS-, or PMA-stimulated human neutrophils upon adhesion to fibronectin. Electron microscopy showed that the morphology of the neutrophils adherent to fibronectin in the presence of various stimuli differed. But in the presence of cytochalasin D, all stimulated neutrophils exhibited a uniform nonspread shape and developed thread-like membrane tubulovesicular extensions (cytonemes) measuring 200 nm in diameter. Simultaneous detection of neutrophil secretory products by mass spectrometry showed that all tested stimuli caused the secretion of MMP-9, a key enzyme in the neutrophil migration. Cytochalasin D impaired the MMP-9 secretion but initiated the release of cathepsin G and other granular bactericides, proinflammatory agents. The release of bactericides apparently occurs through the formation, shedding, and lysis of cytonemes. The production of alkaloids which modify neutrophil responses to stimulation via actin depolymerization may be part of the strategy of pathogen invasion.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mold Alkaloid Cytochalasin D Modifies the Morphology and Secretion of fMLP-, LPS-, or PMA-Stimulated Neutrophils upon Adhesion to Fibronectin

Galkina

Федорова

Serebryakova

et al. 2017

Mediators of Inflammation

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“…Proteome analysis revealed that cytonemes contain the bactericides of primary (myeloperoxidase, cathepsin G, and defensins) and secondary (lactoferrin, lipocalin) secretory granules of neutrophils and a number of cytosolic proteins. Cytosolic proteins include: (i) energy metabolism enzymes such as a number of glycolytic enzymes and transketolase and glucose-6phosphate dehydrogenase; (ii) actin cytoskeleton proteins beta and/or gamma actin, L-plastin and moesin; (iii) S100 proteins and annexin 1 [5,9,29]. Electron microscopy is the most suitable technique for studying so small structures and its interactions with bacteria, but the application of these methods is associated with considerable difficulties.…”

Section: Structure Composition and Size Of Cytonemesmentioning

confidence: 99%

“…Binding of bacteria by cytonemes does not lead to next phagocytosis of microbes, but rather causes shedding of cytonemes with bound bacteria from the cell surface. The destruction of bacteria can occur due to the release of bactericidal agents from the membrane vesicles and tubules that make up cytonemes [29]. Extracellular binding of microbes by cytonemes has several advantages compared with phagocytosis.…”

Section: How Cytonemes Scavenge Microbes: Advantages Over Phagocytosismentioning

confidence: 99%

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Cytonemes Versus Neutrophil Extracellular Traps in the Fight of Neutrophils with Microbes

Galkina

Федорова

Golenkina

et al. 2020

IJMS

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Neutrophils can phagocytose microorganisms and destroy them intracellularly using special bactericides located in intracellular granules. Recent evidence suggests that neutrophils can catch and kill pathogens extracellularly using the same bactericidal agents. For this, live neutrophils create a cytoneme network, and dead neutrophils provide chromatin and proteins to form neutrophil extracellular traps (NETs). Cytonemes are filamentous tubulovesicular secretory protrusions of living neutrophils with intact nuclei. Granular bactericides are localized in membrane vesicles and tubules of which cytonemes are composed. NETs are strands of decondensed DNA associated with histones released by died neutrophils. In NETs, bactericidal neutrophilic agents are adsorbed onto DNA strands and are not covered with a membrane. Cytonemes and NETs occupy different places in protecting the body against infections. Cytonemes can develop within a few minutes at the site of infection through the action of nitric oxide or actin-depolymerizing alkaloids of invading microbes. The formation of NET in vitro occurs due to chromatin decondensation resulting from prolonged activation of neutrophils with PMA (phorbol 12-myristate 13-acetate) or other stimuli, or in vivo due to citrullination of histones with peptidylarginine deiminase 4. In addition to antibacterial activity, cytonemes are involved in cell adhesion and communications. NETs play a role in autoimmunity and thrombosis.

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Cytonemes and the dispersion of morphogens

Kornberg

2014

WIREs Developmental Biology

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Filopodia are cellular protrusions that have been implicated in many types of mechanosensory activities. Morphogens are signaling proteins that regulate the patterned development of embryos and tissues. Both have long histories that date to the beginnings of cell and developmental biology in the early 20th century, but recent findings tie specialized filopodia called cytonemes to morphogen movement and morphogen signaling. This review explores the conceptual and experimental background for a model of paracrine signaling in which the exchange of morphogens between cells is directed to sites where cytonemes directly link cells that produce morphogens to cells that receive and respond to them.

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Membrane tubulovesicular extensions (cytonemes)

Cited by 14 publications

References 127 publications

Mold Alkaloid Cytochalasin D Modifies the Morphology and Secretion of fMLP-, LPS-, or PMA-Stimulated Neutrophils upon Adhesion to Fibronectin

Mold Alkaloid Cytochalasin D Modifies the Morphology and Secretion of fMLP-, LPS-, or PMA-Stimulated Neutrophils upon Adhesion to Fibronectin

Cytonemes Versus Neutrophil Extracellular Traps in the Fight of Neutrophils with Microbes

Cytonemes and the dispersion of morphogens

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