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Special Issue "Molecular Regulation of the Endomembrane System 2.0"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 31 May 2021.

Special Issue Editor

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue, “Molecular Regulation of the Endomembrane System”.

One striking observation in eukaryotic cells is that over time, their organelles maintain a remarkably constant size and shape despite high levels of biochemical activity. In the early secretory pathway, for example, proteins synthesized in the endoplasmic reticulum (ER) but which are destined for secretion are constantly packaged into membrane transport carriers that leave the ER and are directed towards the Golgi complex. The fact that the ER maintains its overall size, shape, and volume tells us that this organelle must receive—from the Golgi complex—an equivalent amount of membrane per unit time. Indeed, if all the organelles in the endomembrane system are to retain their functionality, such counterbalancing of the membrane flow must exist between all compartments that communicate with each other. This control of the endomembrane system is achieved through a variety of factors, including the activity of proteins and lipids resident in each compartment, as well as through long-range signaling events across the cell and linkage to the cytoskeleton. What is also clear is that perturbation of transport pathways between organelles, manifested in a number of diseases, results in aberrant organelle function and morphology.

In this Special Issue entitled “Molecular Regulation of the Endomembrane System 2.0”, we are seeking novel research or review articles highlighting the variety of machinery and regulatory mechanisms used in membrane traffic, with specific regard to how membrane flux is controlled and how it determines the identity and function of organelles. Also relevant is how dysfunctional trafficking events have implications in disease. We are open to articles addressing the molecular control of membrane traffic in a variety of model systems. We look forward to receiving your contributions to this exciting Special Issue.

Dr. Jeremy Simpson
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • membrane traffic
  • secretory pathway
  • endocytic pathway
  • organelle identity
  • coat proteins
  • small GTPases
  • lipids and phosphoinositides
  • endoplasmic reticulum
  • Golgi complex endosomal system
  • cytoskeleton
  • signalling pathways
  • disease, infection, and membrane traffic

Published Papers (2 papers)

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Research

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Open AccessArticle
The p24 Complex Contributes to Specify Arf1 for COPI Coat Selection
Int. J. Mol. Sci. 2021, 22(1), 423; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22010423 - 03 Jan 2021
Viewed by 595
Abstract
Golgi trafficking depends on the small GTPase Arf1 which, upon activation, drives the assembly of different coats onto budding vesicles. Two related types of guanine nucleotide exchange factors (GEFs) activate Arf1 at different Golgi sites. In yeast, Gea1 in the cis-Golgi and [...] Read more.
Golgi trafficking depends on the small GTPase Arf1 which, upon activation, drives the assembly of different coats onto budding vesicles. Two related types of guanine nucleotide exchange factors (GEFs) activate Arf1 at different Golgi sites. In yeast, Gea1 in the cis-Golgi and Gea2 in the medial-Golgi activate Arf1 to form COPI-­coated vesicles for retrograde cargo sorting, whereas Sec7 generates clathrin/adaptor­-coated vesicles at the trans-Golgi network (TGN) for forward cargo transport. A central question is how the same activated Arf1 protein manages to assemble different coats depending on the donor Golgi compartment. A previous study has postulated that the interaction between Gea1 and COPI would channel Arf1 activation for COPI vesicle budding. Here, we found that the p24 complex, a major COPI vesicle cargo, promotes the binding of Gea1 with COPI by increasing the COPI association to the membrane independently of Arf1 activation. Furthermore, the p24 complex also facilitates the interaction of Arf1 with its COPI effector. Therefore, our study supports a mechanism by which the p24 complex contributes to program Arf1 activation by Gea1 for selective COPI coat assembly at the cis-Golgi compartment. Full article
(This article belongs to the Special Issue Molecular Regulation of the Endomembrane System 2.0)
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Review

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Open AccessReview
The Endosomal Recycling Pathway—At the Crossroads of the Cell
Int. J. Mol. Sci. 2020, 21(17), 6074; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21176074 - 23 Aug 2020
Cited by 3 | Viewed by 825
Abstract
The endosomal recycling pathway lies at the heart of the membrane trafficking machinery in the cell. It plays a central role in determining the composition of the plasma membrane and is thus critical for normal cellular homeostasis. However, defective endosomal recycling has been [...] Read more.
The endosomal recycling pathway lies at the heart of the membrane trafficking machinery in the cell. It plays a central role in determining the composition of the plasma membrane and is thus critical for normal cellular homeostasis. However, defective endosomal recycling has been linked to a wide range of diseases, including cancer and some of the most common neurological disorders. It is also frequently subverted by many diverse human pathogens in order to successfully infect cells. Despite its importance, endosomal recycling remains relatively understudied in comparison to the endocytic and secretory transport pathways. A greater understanding of the molecular mechanisms that support transport through the endosomal recycling pathway will provide deeper insights into the pathophysiology of disease and will likely identify new approaches for their detection and treatment. This review will provide an overview of the normal physiological role of the endosomal recycling pathway, describe the consequences when it malfunctions, and discuss potential strategies for modulating its activity. Full article
(This article belongs to the Special Issue Molecular Regulation of the Endomembrane System 2.0)
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