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Cells
Special Issues
Molecular Mechanisms and Biological Roles of Alternative Autophagy
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Special Issue "Molecular Mechanisms and Biological Roles of Alternative Autophagy"

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

Deadline for manuscript submissions: 31 January 2024 | Viewed by 1226

Special Issue Editor

Prof. Dr. Shigeomi Shimizu

E-Mail Website
Guest Editor
Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima Bunkyo-ku, Tokyo 113-8510, Japan
Interests: alternative autophagy; cell death; Golgi function; mitochondria; neurodegenerative diseases

Special Issue Information

Dear  Colleagues,

Over the past two decades, studies on canonical autophagy have expanded from molecular mechanisms to human diseases. However, recent studies have revealed the existence of another type of autophagy mechanism, namely alternative autophagy or Golgi-membrane-associated degradation (GOMED). Alternative autophagy is different from canonical autophagy in terms of the molecules involved, membrane sources, and substrates degraded. Therefore, alternative autophagy is a different proteolysis mechanism from canonical autophagy, and importantly, it is shown to be involved in a wide variety of physiological events.

This Special Issue will focus on molecular mechanisms of alternative autophagy, how to monitor alternative autophagy, which molecules are degraded, the physiological roles, and related human diseases.

Prof. Dr. Shigeomi Shimizu
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 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

  • alternative autophagy
  • GOMED
  • Golgi
  • proteolysis

Published Papers (1 paper)

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Research

28 pages, 3658 KiB  
Article
Neuronal atg1 Coordinates Autophagy Induction and Physiological Adaptations to Balance mTORC1 Signalling
by
Athanasios Metaxakis
,
Michail Pavlidis
and
Nektarios Tavernarakis
Cells 2023, 12(16), 2024; https://doi.org/10.3390/cells12162024 - 08 Aug 2023
Viewed by 915
Abstract
The mTORC1 nutrient-sensing pathway integrates metabolic and endocrine signals into the brain to evoke physiological responses to food deprivation, such as autophagy. Nevertheless, the impact of neuronal mTORC1 activity on neuronal circuits and organismal metabolism remains obscure. Here, we show that mTORC1 inhibition [...] Read more.
The mTORC1 nutrient-sensing pathway integrates metabolic and endocrine signals into the brain to evoke physiological responses to food deprivation, such as autophagy. Nevertheless, the impact of neuronal mTORC1 activity on neuronal circuits and organismal metabolism remains obscure. Here, we show that mTORC1 inhibition acutely perturbs serotonergic neurotransmission via proteostatic alterations evoked by the autophagy inducer atg1. Neuronal ATG1 alters the intracellular localization of the serotonin transporter, which increases the extracellular serotonin and stimulates the 5HTR7 postsynaptic receptor. 5HTR7 enhances food-searching behaviour and ecdysone-induced catabolism in Drosophila. Along similar lines, the pharmacological inhibition of mTORC1 in zebrafish also stimulates food-searching behaviour via serotonergic activity. These effects occur in parallel with neuronal autophagy induction, irrespective of the autophagic activity and the protein synthesis reduction. In addition, ectopic neuronal atg1 expression enhances catabolism via insulin pathway downregulation, impedes peptidergic secretion, and activates non-cell autonomous cAMP/PKA. The above exert diverse systemic effects on organismal metabolism, development, melanisation, and longevity. We conclude that neuronal atg1 aligns neuronal autophagy induction with distinct physiological modulations, to orchestrate a coordinated physiological response against reduced mTORC1 activity. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Biological Roles of Alternative Autophagy)
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