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Related Concept Videos

Golgi Apparatus01:49

Golgi Apparatus

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As they leave the Endoplasmic Reticulum (ER), properly folded and assembled proteins are selectively packaged into vesicles. These vesicles are transported by microtubule-based motor proteins and fuse together to form vesicular tubular clusters, subsequently arriving at the Golgi apparatus, a eukaryotic endomembrane organelle that often has a distinctive ribbon-like appearance.
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Golgi Apparatus01:09

Golgi Apparatus

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Properly folded and assembled proteins are selectively packaged into vesicles that exit the ER. Motor proteins transport these vesicles to the Golgi apparatus for adding modifications that make these proteins functional at their destination.
The Golgi apparatus is a eukaryotic organelle that has a distinctive ribbon-like appearance. It is a primary sorting and dispatch station for cargo arriving from the ER. Newly arriving vesicles enter the cis face of the Golgi, closest to the ER, and are...
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Vesicular Tubular Clusters01:45

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After budding out from the ER membrane, some COPII vesicles lose their coat and fuse with one another to form larger vesicles and interconnected tubules called vesicular tubular clusters or VTCs. These clusters constitute a compartment at the ER-Golgi interface known as ERGIC (Endoplasmic Reticulum Golgi Intermediate Compartment). The ERGIC is a mobile membrane-bound cargo transport system that sorts proteins secreted from ER and delivers them to the Golgi.
With the help of motor proteins such...
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Protein Translocation Machinery on the ER Membrane01:28

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The translocon complex situated on the ER membrane is the main gateway for the protein secretory pathway. It facilitates the transport of nascent peptides into the ER lumen and their insertion into the ER membrane.
Sec61 protein conducting channel
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Transport Across the Golgi01:26

Transport Across the Golgi

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While it is unclear how molecules move between adjacent Golgi cisternae, it is apparent that the molecules move from cis- cisterna, the entry face, to the trans- cisterna, the exit face. Experiments initially suggested vesicles that bud from one cisterna and fuse with the next cisterna to transport proteins between the cisternae. This vesicular transport model describes the Golgi apparatus as a relatively static structure with a unique enzyme composition in each cisterna. Molecules are...
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GPI Anchoring of Proteins in the ER Membrane01:29

GPI Anchoring of Proteins in the ER Membrane

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GPI-anchoring is a post-translational, reversible protein modification that is ubiquitous in eukaryotes. Such proteins are primarily present on the exoplasmic leaflet of the plasma membrane.
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Quantitative Localization of a Golgi Protein by Imaging Its Center of Fluorescence Mass
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STING Operation at the ER/Golgi Interface.

Tomohiko Taguchi1,2, Kojiro Mukai1, Eiko Takaya1

  • 1Laboratory of Organelle Pathophysiology, Department of Integrative Life Sciences, Graduate School of Life Sciences, Tohoku University, Sendai, Japan.

Frontiers in Immunology
|May 20, 2021
PubMed
Summary

Cytosolic DNA triggers immune responses via cGAS-STING. Retrograde membrane traffic from Golgi to ER is crucial for silencing this pathway, and its defects cause COPA syndrome.

Keywords:
COPA syndromeSAVISTINGSTING regulation by membrane trafficinnate immunitypalmitoylationretrograde membrane traffictrans-Golgi network

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Cytosolic DNA, from self or pathogens, activates innate immunity.
  • The cyclic GMP-AMP (cGAMP) synthase (cGAS)-stimulator of interferon genes (STING) pathway is central to this response.
  • STING, an ER-resident protein, translocates to the Golgi upon activation, initiating inflammatory signaling.

Purpose of the Study:

  • To review the regulation of STING signaling by membrane trafficking.
  • To highlight the role of retrograde membrane traffic from the Golgi to the ER in STING pathway silencing.
  • To discuss the implications of impaired retrograde traffic in autoinflammatory diseases.

Main Methods:

  • Literature review focusing on STING regulation and membrane traffic.
  • Analysis of studies investigating STING localization and function.
  • Examination of genetic defects affecting membrane transport in disease.

Main Results:

  • STING activation leads to its translocation from the ER to the Golgi.
  • Retrograde membrane traffic from the Golgi back to the ER is essential for attenuating STING signaling.
  • Defects in this retrograde pathway, particularly involving coatomer protein complex subunit α (COP-α), are linked to COPA syndrome.

Conclusions:

  • Membrane traffic, especially retrograde transport, plays a critical role in controlling STING-mediated immune responses.
  • Dysregulation of STING by aberrant membrane traffic contributes to autoinflammatory conditions like COPA syndrome.
  • Targeting membrane trafficking pathways may offer therapeutic strategies for STING-related disorders.