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Cells
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Autophagy Genes—Biological Functions
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Autophagy Genes—Biological Functions

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 5279

Special Issue Editors

Prof. Dr. Sabah Hussain

E-Mail Website
Collection Editor
Department of Medicine, Division of Experimental Medicine, McGill University Health Centre, Montreal, QC, Canada
Interests: vascular biology; angiogenesis; cell signaling; angiopoietins; tyrosine kinase receptors; endothelium; cell proliferation; cell differentiation; micro-RNAs; long noncoding RNAs
Special Issues, Collections and Topics in MDPI journals
Dr. Gilles Gouspillou

E-Mail Website
Collection Editor
Department of Human Kinetics, University of Quebec, Montreal, QC, Canada
Interests: mitochondrial dynamics and mitophagy; muscle physiology; sarcopenia; mitochondrial biology
Dr. Jean-Philippe Leduc-Gaudet

E-Mail Website
Collection Editor
Department of Biomedical Science, University of Padova, Padova, Italy
Interests: physiology; mitochondria; skeletal muscle; autophagy; aging process; metabolic complication; cell signaling

Special Issue Information

Dear Colleagues,

Autophagy is a process through which damaged or unnecessary cellular components are degraded by lysosomes. A specific form of autophagy, macroautophagy, is characterized by the formation of double-membrane vesicles that surround organelles, portions of cytoplasm, glycogen, and protein aggregates and deliver them to the lysosomes for degradation. Autophagy generally plays a critical pro-survival role in cellular homeostasis by removing accumulated debris and by regulating adaptation to metabolic stress. However, under specific conditions, autophagy may trigger cell death and promote cancer progression. Autophagy-related (ATG) proteins are required throughout the multiple stages of autophagosome formation in “canonical” autophagy, including initiation and nucleation of isolation membrane, elongation, autophagosome closure around the cargo, autophagosome docking and fusion with the lysosome, and degradation of the cargo by lysosomal enzymes. ATG proteins were first identified in yeast and are well-conserved across organisms. Recent studies have revealed that they are also involved in “non-canonical” functions that do not involve classical autophagosome formation or do not terminate with autophagosome-lysosome fusion. These functions are critical to host–pathogen interactions and immune signaling. This Special Issue will address various biological functions of several different autophagy-related genes in relation to normal cellular physiology and the pathophysiology of human disease.

Prof. Dr. Sabah Hussain
Dr. Gilles Gouspillou
Dr. Jean-Philippe Leduc-Gaudet
Guest Editors

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 submissions that pass pre-check are 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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • infection
  • Autophagy Genes
  • Cell Death
  • metabolism
  • neurodegenerative diseases  
  • skeletal muscle 
  • vesicular trafficking 
  • proliferation  
  • phagocytosis  
  • exocytosis  
  • inflammation  
  • cell survival

Published Papers (2 papers)

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Research

17 pages, 40793 KiB  
Article
Analysis of the Compositional Features and Codon Usage Pattern of Genes Involved in Human Autophagy
by Zarnain Jamil, Arif Uddin, Syed Sahajada Mahafujul Alam, Arijit Samanta, Nojood Altwaijry, Mohd Ahmar Rauf, Safdar Ali, Mohd Shahnawaz Khan, Muhammad Nadeem Asghar and Mehboob Hoque
Cells 2022, 11(20), 3203; https://doi.org/10.3390/cells11203203 - 12 Oct 2022
Cited by 5 | Viewed by 2049
Abstract
Autophagy plays an intricate role in paradigmatic human pathologies such as cancer, and neurodegenerative, cardiovascular, and autoimmune disorders. Autophagy regulation is performed by a set of autophagy-related (ATG) genes, first recognized in yeast genome and subsequently identified in other species, including [...] Read more.
Autophagy plays an intricate role in paradigmatic human pathologies such as cancer, and neurodegenerative, cardiovascular, and autoimmune disorders. Autophagy regulation is performed by a set of autophagy-related (ATG) genes, first recognized in yeast genome and subsequently identified in other species, including humans. Several other genes have been identified to be involved in the process of autophagy either directly or indirectly. Studying the codon usage bias (CUB) of genes is crucial for understanding their genome biology and molecular evolution. Here, we examined the usage pattern of nucleotide and synonymous codons and the influence of evolutionary forces in genes involved in human autophagy. The coding sequences (CDS) of the protein coding human autophagy genes were retrieved from the NCBI nucleotide database and analyzed using various web tools and software to understand their nucleotide composition and codon usage pattern. The effective number of codons (ENC) in all genes involved in human autophagy ranges between 33.26 and 54.6 with a mean value of 45.05, indicating an overall low CUB. The nucleotide composition analysis of the autophagy genes revealed that the genes were marginally rich in GC content that significantly influenced the codon usage pattern. The relative synonymous codon usage (RSCU) revealed 3 over-represented and 10 under-represented codons. Both natural selection and mutational pressure were the key forces influencing the codon usage pattern of the genes involved in human autophagy. Full article
(This article belongs to the Special Issue Autophagy Genes—Biological Functions)
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21 pages, 4819 KiB  
Article
The Degradation of TMEM166 by Autophagy Promotes AMPK Activation to Protect SH-SY5Y Cells Exposed to MPP+
by Zhaozhong Liao, Zunshuang Gong, Zhe Wang, Weiyan Yang, Wenjing Liu, Lin Hou, Xiaokun Liu, Junnan Hua, Bin Wang and Ning Li
Cells 2022, 11(17), 2706; https://doi.org/10.3390/cells11172706 - 30 Aug 2022
Cited by 6 | Viewed by 2661
Abstract
Neuronal oxidative stress caused by mitochondrial dysfunction plays a crucial role in the development of Parkinson’s disease (PD). Growing evidence shows that autophagy confers neuroprotection in oxidative-stress-associated PD. This work aims to investigate the involvement of TMEM166, an endoplasmic-reticulum-localized autophagy-regulating protein, in the [...] Read more.
Neuronal oxidative stress caused by mitochondrial dysfunction plays a crucial role in the development of Parkinson’s disease (PD). Growing evidence shows that autophagy confers neuroprotection in oxidative-stress-associated PD. This work aims to investigate the involvement of TMEM166, an endoplasmic-reticulum-localized autophagy-regulating protein, in the process of PD-associated oxidative stress through the classic cellular PD model of neuroblastoma SH-SY5Y cells exposed to 1-methyl-4-phenylpyridinium (MPP+). Reactive oxygen species (ROS) production and mitochondrial membrane potential were checked to assess the oxidative stress induced by MPP+ and the cellular ATP generated was determined to evaluate mitochondrial function. The effect on autophagy induction was evaluated by analyzing p62 and LC3-II/I expression and by observing the LC3 puncta and the colocalization of LC3 with LAMP1/ LAMP2. The colocalization of mitochondria with LC3, the colocalization of Tom20 with LAMP1 and Tom20 expression were analyzed to evaluate mitophagy. We found that TMEM166 is up-regulated in transcript levels, but up-regulated first and then down-regulated by autophagic degradation in protein levels upon MPP+-treatment. Overexpression of TMEM166 induces mitochondria fragmentation and dysfunction and exacerbates MPP+-induced oxidative stress and cell viability reduction. Overexpression of TMEM166 is sufficient to induce autophagy and mitophagy and promotes autophagy and mitophagy under MPP+ treatment, while knockdown of TMEM166 inhibits basal autophagic degradation. In addition, overexpressed TMEM166 suppresses AMPK activation, while TMEM166 knockdown enhances AMPK activation. Pharmacological activation of AMPK alleviates the exacerbation of oxidative stress induced by TMEM166 overexpression and increases cell viability, while pharmacological inhibition mitophagy aggravates the oxidative stress induced by MPP+ treatment combined with TMEM166 overexpression. Finally, we find that overexpressed TMEM166 partially localizes to mitochondria and, simultaneously, the active AMPK in mitochondria is decreased. Collectively, these findings suggest that TMEM166 can translocate from ER to mitochondria and inhibit AMPK activation and, in response to mitochondrial oxidative stress, neuronal cells choose to up-regulate TMEM166 to promote autophagy/mitophagy; then, the enhancing autophagy/mitophagy degrades the TMEM166 to activate AMPK, by the two means to maintain cell survival. The continuous synthesis and degradation of TMEM166 in autophagy/mitochondria flux suggest that TMEM166 may act as an autophagy/mitochondria adaptor. Full article
(This article belongs to the Special Issue Autophagy Genes—Biological Functions)
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