The Exocyst at a Glance

Wu, Bin; Guo, Wei

doi:10.1242/jcs.156398

Cited by 224 publications

(265 citation statements)

References 146 publications

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“…One such tether is the exocyst, an evolutionary conserved, octameric complex that targets recycling endosomes or secretory vesicles to the PM prior to fusion ( Figure 5). This process is of crucial importance as it is involved in cytokinesis, cell migration, ciliogenesis and polarized membrane traffic (Wu and Guo 2015).…”

Section: Exocyst Tethering In Endosomal Exocytosis Is Regulated By Enmentioning

confidence: 99%

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A phosphoinositide conversion mechanism for exit from endosomes

Ketel¹,

Krauß²,

Nicot³

et al. 2016

Nature

161

177

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I owe special thanks to Marnix Wieffer and Michael Krauß, who spent a lot of time helping me to get started in the lab, to overcome numerous experimental problem, I was not sure how to deal with, and frequently joined in discussions about my project with excellent advice. I am really grateful for your experimental support, Michael, and the time you invested in the project during our paper revision.Further, I would like to thank Jocelyn Laporte and his group, especially Anne-Sophie Nicot, at the IGBMC in Strasbourg for their support and a very fruitful collaboration, and Carsten Schultz and his group at the EMBL in Heidelberg for their support and constant supply with PIP/AMs. I owe special thanks to Dmytro Puchkov for the ultrastructural analysis and Eberhard Krause for mass spectrometry done within this project. I also need to acknowledge Markus Wenk and Federico Torta at the Singapore Lipidomics Incubator for joining the project at a very late stage, when we urgently needed help from lipidomics specialists. It was a pity that experiments did not work out as planned.I would further like to express my gratitude to two very skilled technicians in the AG Haucke lab: Silke Zillmann and Delia Löwe. Without your help it would have been impossible to achieve so much within the limited amount of time I had during the paper revision. by VPS34-IN1 treatment................................................... 52 2.3.11 Fluorescence microscopy................................................................................. 53 2.3.12 Flow cytometry............................................................................................ III SummaryPhosphoinositides (PIs) are a minor class of short-lived phospholipids that serve as crucial signposts of membrane identity. Thereby, PIs full fill important functions in cell signaling and membrane transport. PI 4-phosphates such as phosphatitylinositol-4-phosphate (PI(4)P) and phosphatitylinositol-4,5-bisphosphate (PI(4,5)P 2 ) are enriched at the plasma membrane (PM), on secretory organelles and lysosomes, while PI 3-phosphates, i.e.phosphatitylinositol-3-phosphate (PI(3)P), are a hallmark of the endosomal system.Directional transport between these compartments, thus, requires regulated PI conversion.However, PI conversion in exit from PI(3)P-enriched endosomes en route to the PI(4)P-and PI(4,5)P 2 -positive PM in endosomal recycling remained unknown.Here, we report that cargo exit from endosomes requires removal of PI(3)P by the PI(3)P 3-phosphatase myotubularin 1 (MTM1), and concomitant PI(4)P synthesis by PI 4-kinase type II α (PI4K2α). Loss of MTM1 causes endosomal accumulation of PI(3)P and PI(3)P effector proteins, i.e. sorting nexins, Kif16b-mediated outward traffic of PI(3)P containing endosomes and sub-plasmalemmal accumulation of exocytosis-deficient endosomes. As PI4K2α associates with MTM1 and thereby facilitates membrane recruitment of MTM1, these phenotypic changes are mimicked by loss of PI4K2α. The conversion of PI(3)P-to-PI(4)P is paralleled by a switch i...

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Section: Exocyst Tethering In Endosomal Exocytosis Is Regulated By Enmentioning

confidence: 99%

“…Association with vSNAREs, i.e.VAMP2/3, t-SNAREs, i.e. Syntaxin 13, and SNAP23/25 couples exocyst tethering to plasma membrane fusion (Wu and Guo 2015).…”

Section: Figure 5: Exocyst Assembly and Vesicle Tetheringmentioning

confidence: 99%

A phosphoinositide conversion mechanism for exit from endosomes

Ketel¹,

Krauß²,

Nicot³

et al. 2016

Nature

161

177

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“…Although skeletal muscle cells express several canonical secretory vesicle transport proteins including specific VAMPs (2–5,7, and 8) and associated t-SNAREs [50], the mechanisms that target VAMP-containing vesicles to particular regions in the plasma membrane to control myokine secretion are largely unknown. In many cell types, the initial stage of vesicle translocation from the Golgi to the periphery involves movement along growing microtubules and/or filamentous or branched actin bundles that radiate towards the plasma membrane[51]. However, most of the actin in skeletal muscle cells is organized into distinct striated fibers and the microtubules are organized in a stable orthogonal lattice comprised of MT bundles [52] suggesting that vesicle transport, docking, and release are likely coordinated in a unique fashion in these cells.…”

Section: Introductionmentioning

confidence: 99%

Muscle as a paracrine and endocrine organ

Giudice

Taylor

2017

Current Opinion in Pharmacology

254

186

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Skeletal muscle cells are highly abundant and metabolically active and are known to ‘communicate’ their energy demands to other organs through active secretion. Muscle-derived secretory proteins include a variety of cytokines and peptides collectively referred to as “myokines” that exert auto-, para- or endocrine effects. Analyses of the skeletal muscle secretome revealed that numerous myokines are secreted in response to contraction or strength training, and that these factors not only regulate energy demand but also contribute to the broad beneficial effects of exercise on cardiovascular, metabolic, and mental health. Herein we review recent studies on the myokines that regulate muscle function and those that mediate cross talk between skeletal muscle and other organs including adipose tissue, liver, pancreas, the cardiovascular system, brain, bones, and skin.

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“…Secretion of MMPs also requires the proper function of the exocytosis machinery. The exocyst, an octameric protein complex consisting of Sec3, Sec5, Sec6, Sec8, Sec10, Sec15, Exo70 and Exo84, mediates the docking of secretory vesicles to the plasma membrane during exocytosis (Wu and Guo, 2015; He and Guo, 2009; Hsu et al, 2004). Recent studies demonstrate that the exocyst is involved in MMP secretion and cell migration (Sakurai-Yageta M et al, 2008; Liu et al, 2009; Lu et al, 2013; Ren and Guo, 2012; Monteiro et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Oncogenic BRAF-Mediated Melanoma Cell Invasion

Liu

Zhang

et al. 2016

Cell Reports

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SUMMARY Melanoma patients with oncogenic BRAFV600E mutation have poor prognoses. While the role of BRAFV600E in tumorigenesis is well established, its involvement in invasion that is clinically observed in melanoma patients, remains a topic of debate. Here we show that BRAFV600E melanoma cells have extensive invasion activity as assayed by degradation of extracellular matrix, and generation of F-actin and cortactin foci that mediate membrane protrusion. Inhibition of BRAFV600E blocks melanoma cell invasion. In a BRAFV600E-driven murine melanoma model or in patients’ tumor biopsies, cortactin foci decrease upon inhibitor treatment. In addition, genome-wide expression analysis shows that a number of invadopodia-related genes are down-regulated after BRAFV600E inhibition. Mechanistically, BRAFV600E induces phosphorylation of cortactin and the exocyst subunit Exo70 through ERK, which regulates actin dynamics and matrix metalloprotease secretion, respectively. Our results provide support for the role of BRAFV600E in metastasis, and suggest that inhibiting invasion is a potential therapeutic strategy against melanoma.

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The Exocyst at a Glance

Cited by 224 publications

References 146 publications

A phosphoinositide conversion mechanism for exit from endosomes

A phosphoinositide conversion mechanism for exit from endosomes

Muscle as a paracrine and endocrine organ

Oncogenic BRAF-Mediated Melanoma Cell Invasion

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