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Cells
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Golgi Apparatus Dysfunction in Disease
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Golgi Apparatus Dysfunction in Disease

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 13483

Special Issue Editor

Dr. Francisco Lázaro-Diéguez

E-Mail Website
Guest Editor
Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
Interests: Golgi apparatus; post-Golgi trafficking; actin cytoskeleton; RhoA; cell adhesion; cell polarity; cell division
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The Golgi apparatus is essential to maintain cellular homeostasis, playing a fundamental role in the modification, package, and transport of proteins and lipids towards their specific targets. This organelle is also involved in the regulation of diverse cellular processes including mitosis, autophagy, and apoptosis.

In most mammalian cells the Golgi is a polarized structure composed of connected stacks of piled, flat, and dynamic cisternae -Golgi ribbon-, where emerging vesicles and tubules are observed mainly at the trans- side. The degree of connection -transient or stable- between cisternae inter -and intra- stacks and the physiological benefits conferred by the particular shape and stacking of Golgi cisternae are unclear. It is considered that this architecture is required for the fine regulation of cargo processing and transport during secretion.

The dynamic structure and functional integrity of the Golgi is determined and finely regulated by the orchestrated contribution of microtubule and actin cytoskeletons, golgins, and Golgi stacking proteins among others. Furthermore, the Golgi organization is also affected in response to cellular stress. Mutations in genes encoding Golgi resident proteins cause genetic diseases that result in membrane trafficking defects (e.g. Wilson disease caused by mutations in the copper transporter ATP7B). In addition, Golgi ribbon fragmentation/stacks dispersion is observed in cancer, infectious, and neurodegenerative diseases, including Amyotrophic Lateral Sclerosis, Alzheimer, and Parkinson.

However, it is not fully understood how impaired Golgi architecture affects its function or whether it is a cause or consequence of disease progression.

This Special Issue will focus on Golgi dysfunction in disease and will collect original research articles and reviews that expand our basic knowledge of the Golgi apparatus.

Dr. Francisco Lázaro-Diéguez
Guest Editor

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Keywords

  • Golgi apparatus
  • Intracellular protein trafficking
  • Cytoskeleton
  • Golgi-resident proteins
  • Cancer
  • Neurodegenerative disease
  • Oxidative stress

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Published Papers (3 papers)

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Research

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19 pages, 7447 KiB  
Article
SLC35A2 Deficiency Promotes an Epithelial-to-Mesenchymal Transition-like Phenotype in Madin–Darby Canine Kidney Cells
by Magdalena Kot, Ewa Mazurkiewicz, Maciej Wiktor, Wojciech Wiertelak, Antonina Joanna Mazur, Andrei Rahalevich, Mariusz Olczak and Dorota Maszczak-Seneczko
Cells 2022, 11(15), 2273; https://doi.org/10.3390/cells11152273 - 23 Jul 2022
Cited by 3 | Viewed by 2592
Abstract
In mammalian cells, SLC35A2 delivers UDP–galactose for galactosylation reactions that take place predominantly in the Golgi lumen. Mutations in the corresponding gene cause a subtype of a congenital disorder of glycosylation (SLC35A2-CDG). Although more and more patients are diagnosed with SLC35A2-CDG, the link [...] Read more.
In mammalian cells, SLC35A2 delivers UDP–galactose for galactosylation reactions that take place predominantly in the Golgi lumen. Mutations in the corresponding gene cause a subtype of a congenital disorder of glycosylation (SLC35A2-CDG). Although more and more patients are diagnosed with SLC35A2-CDG, the link between defective galactosylation and disease symptoms is not fully understood. According to a number of reports, impaired glycosylation may trigger the process of epithelial-to-mesenchymal transition (EMT). We therefore examined whether the loss of SLC35A2 activity would promote EMT in a non-malignant epithelial cell line. For this purpose, we knocked out the SLC35A2 gene in Madin–Darby canine kidney (MDCK) cells. The resulting clones adopted an elongated, spindle-shaped morphology and showed impaired cell–cell adhesion. Using qPCR and western blotting, we revealed down-regulation of E-cadherin in the knockouts, while the fibronectin and vimentin levels were elevated. Moreover, the knockout cells displayed reorganization of vimentin intermediate filaments and altered subcellular distribution of a vimentin-binding protein, formiminotransferase cyclodeaminase (FTCD). Furthermore, depletion of SLC35A2 triggered Golgi compaction. Finally, the SLC35A2 knockouts displayed increased motility and invasiveness. In conclusion, SLC35A2-deficient MDCK cells showed several hallmarks of EMT. Our findings point to a novel role for SLC35A2 as a gatekeeper of the epithelial phenotype. Full article
(This article belongs to the Special Issue Golgi Apparatus Dysfunction in Disease)
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Review

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12 pages, 2094 KiB  
Review
Golgi Dysfunctions in Ciliopathies
by Justine Masson and Vincent El Ghouzzi
Cells 2022, 11(18), 2773; https://doi.org/10.3390/cells11182773 - 6 Sep 2022
Cited by 6 | Viewed by 2267
Abstract
The Golgi apparatus (GA) is essential for intracellular sorting, trafficking and the targeting of proteins to specific cellular compartments. Anatomically, the GA spreads all over the cell but is also particularly enriched close to the base of the primary cilium. This peculiar organelle [...] Read more.
The Golgi apparatus (GA) is essential for intracellular sorting, trafficking and the targeting of proteins to specific cellular compartments. Anatomically, the GA spreads all over the cell but is also particularly enriched close to the base of the primary cilium. This peculiar organelle protrudes at the surface of almost all cells and fulfills many cellular functions, in particular during development, when a dysfunction of the primary cilium can lead to disorders called ciliopathies. While ciliopathies caused by loss of ciliated proteins have been extensively documented, several studies suggest that alterations of GA and GA-associated proteins can also affect ciliogenesis. Here, we aim to discuss how the loss-of-function of genes coding these proteins induces ciliary defects and results in ciliopathies. Full article
(This article belongs to the Special Issue Golgi Apparatus Dysfunction in Disease)
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18 pages, 1120 KiB  
Review
Dance of The Golgi: Understanding Golgi Dynamics in Cancer Metastasis
by Rakhee Bajaj, Amanda N. Warner, Jared F. Fradette and Don L. Gibbons
Cells 2022, 11(9), 1484; https://doi.org/10.3390/cells11091484 - 28 Apr 2022
Cited by 23 | Viewed by 5229
Abstract
The Golgi apparatus is at the center of protein processing and trafficking in normal cells. Under pathological conditions, such as in cancer, aberrant Golgi dynamics alter the tumor microenvironment and the immune landscape, which enhances the invasive and metastatic potential of cancer cells. [...] Read more.
The Golgi apparatus is at the center of protein processing and trafficking in normal cells. Under pathological conditions, such as in cancer, aberrant Golgi dynamics alter the tumor microenvironment and the immune landscape, which enhances the invasive and metastatic potential of cancer cells. Among these changes in the Golgi in cancer include altered Golgi orientation and morphology that contribute to atypical Golgi function in protein trafficking, post-translational modification, and exocytosis. Golgi-associated gene mutations are ubiquitous across most cancers and are responsible for modifying Golgi function to become pro-metastatic. The pharmacological targeting of the Golgi or its associated genes has been difficult in the clinic; thus, studying the Golgi and its role in cancer is critical to developing novel therapeutic agents that limit cancer progression and metastasis. In this review, we aim to discuss how disrupted Golgi function in cancer cells promotes invasion and metastasis. Full article
(This article belongs to the Special Issue Golgi Apparatus Dysfunction in Disease)
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