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      Regulation of the Autophagic Bcl-2/Beclin 1 Interaction

      review-article
      Author(s): * , , *
      Publication date (Electronic):
      Journal: Cells
      Publisher: MDPI
      Keywords: autophagy, Bcl-2, Bcl-XL, Mcl-1, Beclin 1, JNK1, DAPK, IP3R, Naf-1, BH3 mimetics

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          Abstract

          Autophagy is an intracellular degradation process responsible for the delivery of cellular material to the lysosomes. One of the key mechanisms for control of autophagy is the modulation of the interaction between the autophagic protein Beclin 1 and the members of the anti-apoptotic Bcl-2 family (e.g., Bcl-2, Bcl-X L and Mcl-1). This binding is regulated by a variety of proteins and compounds that are able to enhance or inhibit the Bcl-2/Beclin 1 interaction in order to repress or activate autophagy, respectively. In this review we will focus on this interaction and discuss its characteristics, relevance and regulation.

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          Mitochondrial autophagy is an HIF-1-dependent adaptive metabolic response to hypoxia.

          Huafeng Zhang, Marta Bosch-Marce, Larissa Shimoda … (2008)
          Autophagy is a process by which cytoplasmic organelles can be catabolized either to remove defective structures or as a means of providing macromolecules for energy generation under conditions of nutrient starvation. In this study we demonstrate that mitochondrial autophagy is induced by hypoxia, that this process requires the hypoxia-dependent factor-1-dependent expression of BNIP3 and the constitutive expression of Beclin-1 and Atg5, and that in cells subjected to prolonged hypoxia, mitochondrial autophagy is an adaptive metabolic response which is necessary to prevent increased levels of reactive oxygen species and cell death.
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            Beclin 1, an autophagy gene essential for early embryonic development, is a haploinsufficient tumor suppressor.

            Zhenyu Yue, Shengkan Jin, Chingwen Yang … (2003)
            The biochemical properties of beclin 1 suggest a role in two fundamentally important cell biological pathways: autophagy and apoptosis. We show here that beclin 1-/- mutant mice die early in embryogenesis and beclin 1+/- mutant mice suffer from a high incidence of spontaneous tumors. These tumors continue to express wild-type beclin 1 mRNA and protein, establishing that beclin 1 is a haploinsufficient tumor suppressor gene. Beclin 1-/- embryonic stem cells have a severely altered autophagic response, whereas their apoptotic response to serum withdrawal or UV light is normal. These results demonstrate that beclin 1 is a critical component of mammalian autophagy and establish a role for autophagy in tumor suppression. They both provide a biological explanation for recent evidence implicating beclin 1 in human cancer and suggest that mutations in other genes operating in this pathway may contribute to tumor formation through deregulation of autophagy.
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              Mitochondria supply membranes for autophagosome biogenesis during starvation.

              Dale Hailey, Angelika Rambold, Prasanna Satpute-Krishnan … (2010)
              Starvation-induced autophagosomes engulf cytosol and/or organelles and deliver them to lysosomes for degradation, thereby resupplying depleted nutrients. Despite advances in understanding the molecular basis of this process, the membrane origin of autophagosomes remains unclear. Here, we demonstrate that, in starved cells, the outer membrane of mitochondria participates in autophagosome biogenesis. The early autophagosomal marker, Atg5, transiently localizes to punctae on mitochondria, followed by the late autophagosomal marker, LC3. The tail-anchor of an outer mitochondrial membrane protein also labels autophagosomes and is sufficient to deliver another outer mitochondrial membrane protein, Fis1, to autophagosomes. The fluorescent lipid NBD-PS (converted to NBD-phosphotidylethanolamine in mitochondria) transfers from mitochondria to autophagosomes. Photobleaching reveals membranes of mitochondria and autophagosomes are transiently shared. Disruption of mitochondria/ER connections by mitofusin2 depletion dramatically impairs starvation-induced autophagy. Mitochondria thus play a central role in starvation-induced autophagy, contributing membrane to autophagosomes. Copyright (c) 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 06 July 2012
                Publication date Collection: September 2012
                Volume: 1
                Issue: 3
                Pages: 284-312
                Affiliations
                Laboratory of Molecular and Cellular Signaling, Department of Cellular and Molecular Medicine, KU Leuven, O/N-1, bus 802, Herestraat 49, Leuven, BE-3000, Belgium; Email: jan.parys@ 123456med.kuleuven.be
                Author notes
                [* ] Authors to whom correspondence should be addressed; Email: jeanpaul.decuypere@ 123456med.kuleuven.be (J.-P.D.); geert.bultynck@ 123456med.kuleuven.be (G.B.); Tel.: +32-16-330-215; Fax: +32-16-330-732.
                Article
                Publisher ID: cells-01-00284
                DOI: 10.3390/cells1030284
                PMC ID: 3901098
                PubMed ID: 24710477
                SO-VID: 5e5bc4b4-b5bd-4a68-b88a-7c2ce610e7ea
                Copyright © © 2012 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 14 May 2012
                Date revision received : 06 June 2012
                Date accepted : 15 June 2012
                Categories
                Subject: Review

                Keywords: autophagy,bcl-2,bcl-xl,mcl-1,beclin 1,jnk1,dapk,ip3r,naf-1,bh3 mimetics
                Data availability:
                Keywords: autophagy, bcl-2, bcl-xl, mcl-1, beclin 1, jnk1, dapk, ip3r, naf-1, bh3 mimetics

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