On the fly: recent progress on autophagy and aging in Drosophila
- 1Biological Research Centre (MTA), Hungarian Academy of Sciences, Hungary
- 2Department of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Hungary
Autophagy ensures the lysosome-mediated breakdown and recycling of self-material, as it not only degrades obsolete or damaged intracellular constituents but also provides building blocks for biosynthetic and energy producing reactions. Studies in animal models including Drosophila revealed that autophagy defects lead to the rapid decline of neuromuscular function, neurodegeneration, sensitivity to stress (such as starvation or oxidative damage), and stem cell loss. Of note, recently identified human Atg gene mutations cause similar symptoms including ataxia and mental retardation. Physiologically, autophagic degradation (flux) is known to decrease during aging, and this defect likely contributes to the development of such age-associated diseases. Many manipulations that extend lifespan (including dietary restriction, reduced TOR kinase signaling, exercise or treatment with various anti-aging substances) require autophagy for their beneficial effect on longevity, pointing to the key role of this housekeeping process. Importantly, genetic (eg. Atg8a overexpression in either neurons or muscle) or pharmacological (eg. feeding rapamycin or spermidine to animals) promotion of autophagy has been successfully used to extend lifespan in Drosophila, suggesting that this intracellular degradation pathway can rejuvenate cells and organisms. In this review, we highlight key discoveries and recent progress in understanding the relationship of autophagy and aging in Drosophila.
Keywords: Aging, Autophagy, Drosophila, Dietary restriction (DR), Spermidine
Received: 11 Apr 2019;
Accepted: 09 Jul 2019.
Edited by:Tassula Proikas-Cezanne, University of Tübingen, Germany
Reviewed by:Brian C. Schaefer, Uniformed Services University of the Health Sciences, United States
Ken Moberg, Emory University School of Medicine, United States
Copyright: © 2019 Maruzs, Simon-Vecsei, Kiss, Csizmadia and Juhász. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Dr. Gábor Juhász, Biological Research Centre (MTA), Hungarian Academy of Sciences, Szeged, Hungary, email@example.com