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      Vital staining for cell death identifies Atg9a-dependent necrosis in developmental bone formation in mouse

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          Abstract

          Programmed cell death has a crucial role in various biological events, including developmental morphogenesis. Recent evidence indicates that necrosis contributes to programmed cell death in addition to apoptosis, but it is unclear whether necrosis acts as a compensatory mechanism for failure of apoptosis or has an intrinsic role during development. In contrast to apoptosis, there have been no techniques for imaging physiological necrosis in vivo. Here we employ vital staining using propidium iodide to identify cells with plasma membrane disruption (necrotic cells) in mouse embryos. We discover a form of necrosis at the bone surface, which does not occur in embryos with deficiency of the autophagy-related gene Atg9a, although it is unaffected by Atg5 knockout. We also find abnormalities of the bone surface in Atg9a knockout mice, suggesting an important role of Atg9a-dependent necrosis in bone surface formation. These findings suggest that necrosis has an active role in developmental morphogenesis.

          Abstract

          Apoptosis occurs in numerous developmental processes but a role for necrosis in development is unclear. Here, the authors develop a detecting system of necrosis in the developing mouse and find a form of necrosis that is dependent on the autophagy-related gene Atg9a.

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          Most cited references29

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          Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009.

          Different types of cell death are often defined by morphological criteria, without a clear reference to precise biochemical mechanisms. The Nomenclature Committee on Cell Death (NCCD) proposes unified criteria for the definition of cell death and of its different morphologies, while formulating several caveats against the misuse of words and concepts that slow down progress in the area of cell death research. Authors, reviewers and editors of scientific periodicals are invited to abandon expressions like 'percentage apoptosis' and to replace them with more accurate descriptions of the biochemical and cellular parameters that are actually measured. Moreover, at the present stage, it should be accepted that caspase-independent mechanisms can cooperate with (or substitute for) caspases in the execution of lethal signaling pathways and that 'autophagic cell death' is a type of cell death occurring together with (but not necessarily by) autophagic vacuolization. This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including 'entosis', 'mitotic catastrophe', 'necrosis', 'necroptosis' and 'pyroptosis'.
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            Autophagosome formation: core machinery and adaptations.

            Eukaryotic cells employ autophagy to degrade damaged or obsolete organelles and proteins. Central to this process is the formation of autophagosomes, double-membrane vesicles responsible for delivering cytoplasmic material to lysosomes. In the past decade many autophagy-related genes, ATG, have been identified that are required for selective and/or nonselective autophagic functions. In all types of autophagy, a core molecular machinery has a critical role in forming sequestering vesicles, the autophagosome, which is the hallmark morphological feature of this dynamic process. Additional components allow autophagy to adapt to the changing needs of the cell.
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              Dynamics and diversity in autophagy mechanisms: lessons from yeast.

              Autophagy is a fundamental function of eukaryotic cells and is well conserved from yeast to humans. The most remarkable feature of autophagy is the synthesis of double membrane-bound compartments that sequester materials to be degraded in lytic compartments, a process that seems to be mechanistically distinct from conventional membrane traffic. The discovery of autophagy in yeast and the genetic tractability of this organism have allowed us to identify genes that are responsible for this process, which has led to the explosive growth of this research field seen today. Analyses of autophagy-related (Atg) proteins have unveiled dynamic and diverse aspects of mechanisms that underlie membrane formation during autophagy.
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                Author and article information

                Journal
                Nat Commun
                Nat Commun
                Nature Communications
                Nature Publishing Group
                2041-1723
                04 November 2016
                2016
                : 7
                : 13391
                Affiliations
                [1 ]Department of Molecular and Cellular Biology, Research Institute of Osaka Medical Center for Cancer and Cardiovascular Diseases , 1-3-2 Nakamichi, Higashinari-ku, Osaka 537-8511, Japan
                [2 ]Laboratory of Molecular Genetics, Department of Medical Genetics, Graduate School of Medicine, Osaka University , 2-2 Yamadaoka, Suita, Osaka 565–0871, Japan
                [3 ]Department of Inflammation Biology, Institute for Enzyme Research, Tokushima University , 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan
                [4 ]Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University , 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan
                Author notes
                Article
                ncomms13391
                10.1038/ncomms13391
                5097171
                27811852
                19fcd1b6-3b06-4b18-998d-0fd9a937f490
                Copyright © 2016, The Author(s)

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 28 July 2016
                : 27 September 2016
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