Syndapin/SDPN-1 is required for endocytic recycling and endosomal actin association in the<i>Caenorhabditis elegans</i>intestine

Gleason, Adenrele M.; Nguyen, Ken; Hall, David H.; Grant, Barth D.

doi:10.1091/mbc.e16-02-0116

Cited by 21 publications

(38 citation statements)

References 61 publications

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“…Our work indicates that microvillus inclusions originate from endocytosis and are dependent on dynamin and Pacsin 2. Interestingly, there is a single report in C. elegans intestine that Syndapin 1 is required for endocytic recycling (Gleason et al, 2016). This report demonstrated that Syndapin 1 was present in early and basolateral Moreover, Syndapin 1 deletion mutants exhibited decreased basolateral recycling transport and accumulation of endosomes positive for early endosome and recycling endosome markers (Gleason et al, 2016).…”

Section: Discussionmentioning

confidence: 95%

“…Interestingly, there is a single report in C. elegans intestine that Syndapin 1 is required for endocytic recycling (Gleason et al, 2016). This report demonstrated that Syndapin 1 was present in early and basolateral Moreover, Syndapin 1 deletion mutants exhibited decreased basolateral recycling transport and accumulation of endosomes positive for early endosome and recycling endosome markers (Gleason et al, 2016). In mammals, the Pacsin 2 protein is primarily implicated in endocytosis, as it associates with multiple endocytic regulators including MICAL-L1, EHD1/mRme-1, and dynamin (Braun et al, 2005;Giridharan et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

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Loss of myosin Vb promotes apical bulk endocytosis in neonatal enterocytes

Engevik

Kaji

Postema

et al. 2019

Journal of Cell Biology

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In patients with inactivating mutations in myosin Vb (Myo5B), enterocytes show large inclusions lined by microvilli. The origin of inclusions in small-intestinal enterocytes in microvillus inclusion disease is currently unclear. We postulated that inclusions in Myo5b KO mouse enterocytes form through invagination of the apical brush border membrane. 70-kD FITC-dextran added apically to Myo5b KO intestinal explants accumulated in intracellular inclusions. Live imaging of Myo5b KO–derived enteroids confirmed the formation of inclusions from the apical membrane. Treatment of intestinal explants and enteroids with Dyngo resulted in accumulation of inclusions at the apical membrane. Inclusions in Myo5b KO enterocytes contained VAMP4 and Pacsin 2 (Syndapin 2). Myo5b;Pacsin 2 double-KO mice showed a significant decrease in inclusion formation. Our results suggest that apical bulk endocytosis in Myo5b KO enterocytes resembles activity-dependent bulk endocytosis, the primary mechanism for synaptic vesicle uptake during intense neuronal stimulation. Thus, apical bulk endocytosis mediates the formation of inclusions in neonatal Myo5b KO enterocytes.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Loss of myosin Vb promotes apical bulk endocytosis in neonatal enterocytes

Engevik

Kaji

Postema

et al. 2019

Journal of Cell Biology

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“…syndapin-1) and PACSIN2 (a.k.a. syndapin-II) (125)(126)(127) , ACAP1 44,128,129 and the SNX-BAR family [130][131][132][133][134] (see also Supplementary Table S1 for a list of membrane-remodelling protein and complexes currently implicated in endosomal recycling). BAR domains are α-helical coiled coils that dimerise to form a banana-shaped structure whose concave surface is lined with positively charged residues that mediate electrostatic interactions with the negatively charged membrane surface 135 (Figure 4).…”

Section: [H1] Tubular Transport Carrier Formationmentioning

confidence: 99%

To degrade or not to degrade: mechanisms and significance of endocytic recycling

Cullen

Steinberg

2018

Nat Rev Mol Cell Biol

449

455

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Newly endocytosed integral cell surface proteins are typically either directed for degradation or subjected to recycling back to the plasma membrane. The sorting of integral cell surface proteins, including signalling receptors, nutrient transporters, ion channels, adhesion molecules and polarity markers, within the endolysosomal network for recycling is increasingly recognized as an essential feature in regulating the complexities of physiology at the cell, tissue and organism levels. Historically, endocytic recycling has been regarded as a relatively passive process, where the majority of internalized integral proteins are recycled via a nonspecific sequence-independent 'bulk membrane flow' pathway. Recent work has increasingly challenged this view. The discovery of sequence-specific sorting motifs and the identification of cargo adaptors and associated coat complexes have begun to uncover the highly orchestrated nature of endosomal cargo recycling, thereby providing new insight into the function and (patho)physiology of this process.

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“…Paradoxically, loss of EHS-1 leads to complete depletion of synaptic vesicles without apparent formation of endosomes, suggesting its function at the plasma membrane, while loss of ITSN-1 results in accumulation of large vesicles in the terminals (Salcini et al, 2001 ). The amphiphysin and syndapin homologs AMPH-1 and SDPN-1 act on early endosomes to regulate cargo recycling (Pant et al, 2009 ; Gleason et al, 2016 ). They are therefore not likely to be directly involved in synaptic vesicle endocytosis from the plasma membrane, although their exact roles are yet to be determined.…”

Section: Caenorhabditis Elegans Neuromuscular Junctionsmentioning

confidence: 99%

Synaptic Vesicle Endocytosis in Different Model Systems

Gan

Watanabe

2018

Front. Cell. Neurosci.

109

120

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Neurotransmission in complex animals depends on a choir of functionally distinct synapses releasing neurotransmitters in a highly coordinated manner. During synaptic signaling, vesicles fuse with the plasma membrane to release their contents. The rate of vesicle fusion is high and can exceed the rate at which synaptic vesicles can be re-supplied by distant sources. Thus, local compensatory endocytosis is needed to replenish the synaptic vesicle pools. Over the last four decades, various experimental methods and model systems have been used to study the cellular and molecular mechanisms underlying synaptic vesicle cycle. Clathrin-mediated endocytosis is thought to be the predominant mechanism for synaptic vesicle recycling. However, recent studies suggest significant contribution from other modes of endocytosis, including fast compensatory endocytosis, activity-dependent bulk endocytosis, ultrafast endocytosis, as well as kiss-and-run. Currently, it is not clear whether a universal model of vesicle recycling exist for all types of synapses. It is possible that each synapse type employs a particular mode of endocytosis. Alternatively, multiple modes of endocytosis operate at the same synapse, and the synapse toggles between different modes depending on its activity level. Here we compile review and research articles based on well-characterized model systems: frog neuromuscular junctions, C. elegans neuromuscular junctions, Drosophila neuromuscular junctions, lamprey reticulospinal giant axons, goldfish retinal ribbon synapses, the calyx of Held, and rodent hippocampal synapses. We will compare these systems in terms of their known modes and kinetics of synaptic vesicle endocytosis, as well as the underlying molecular machineries. We will also provide the future development of this field.

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Syndapin/SDPN-1 is required for endocytic recycling and endosomal actin association in theCaenorhabditis elegansintestine

Cited by 21 publications

References 61 publications

Loss of myosin Vb promotes apical bulk endocytosis in neonatal enterocytes

Loss of myosin Vb promotes apical bulk endocytosis in neonatal enterocytes

To degrade or not to degrade: mechanisms and significance of endocytic recycling

Synaptic Vesicle Endocytosis in Different Model Systems

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