دورية أكاديمية
Mitochondria shed their outer membrane in response to infection-induced stress.
| العنوان: | Mitochondria shed their outer membrane in response to infection-induced stress. |
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| المؤلفون: | Li X; Max Planck Institute for Biology of Ageing, Cologne, Germany., Straub J; Max Planck Institute for Biology of Ageing, Cologne, Germany., Medeiros TC; Max Planck Institute for Biology of Ageing, Cologne, Germany., Mehra C; Max Planck Institute for Biology of Ageing, Cologne, Germany., den Brave F; Institute of Biochemistry and Molecular Biology, Medical Faculty, University of Bonn, Bonn, Germany., Peker E; Institute of Biochemistry, University of Cologne, Cologne, Germany., Atanassov I; Max Planck Institute for Biology of Ageing, Cologne, Germany., Stillger K; Institute of Biochemistry, University of Cologne, Cologne, Germany., Michaelis JB; Institute of Biochemistry II, Faculty of Medicine, Goethe University, Frankfurt am Main, Germany., Burbridge E; Patrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast, Northern Ireland.; Instituto Gulbenkian de Ciência, Oeiras, Portugal., Adrain C; Patrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast, Northern Ireland.; Instituto Gulbenkian de Ciência, Oeiras, Portugal., Münch C; Institute of Biochemistry II, Faculty of Medicine, Goethe University, Frankfurt am Main, Germany., Riemer J; Institute of Biochemistry, University of Cologne, Cologne, Germany.; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany., Becker T; Institute of Biochemistry and Molecular Biology, Medical Faculty, University of Bonn, Bonn, Germany., Pernas LF; Max Planck Institute for Biology of Ageing, Cologne, Germany.; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany. |
| المصدر: | Science (New York, N.Y.) [Science] 2022 Jan 14; Vol. 375 (6577), pp. eabi4343. Date of Electronic Publication: 2022 Jan 14. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Association for the Advancement of Science Country of Publication: United States NLM ID: 0404511 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1095-9203 (Electronic) Linking ISSN: 00368075 NLM ISO Abbreviation: Science Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Original Publication: New York, N.Y. : [s.n.] 1880- |
| مواضيع طبية MeSH: | Mitochondrial Membranes/*physiology , Mitochondrial Precursor Protein Import Complex Proteins/*metabolism , Protozoan Proteins/*metabolism , Toxoplasma/*physiology, Animals ; Cell Line ; GTP Phosphohydrolases/metabolism ; Humans ; Intracellular Membranes/physiology ; Intracellular Membranes/ultrastructure ; Mice ; Mitochondrial Membrane Transport Proteins/metabolism ; Mitochondrial Membranes/ultrastructure ; Mitochondrial Proteins/metabolism ; Protein Binding ; Stress, Physiological ; Toxoplasma/growth & development ; Toxoplasma/ultrastructure ; Toxoplasmosis/parasitology ; Vacuoles/physiology ; Vacuoles/ultrastructure |
| مستخلص: | The outer mitochondrial membrane (OMM) is essential for cellular homeostasis. Yet little is known of the mechanisms that remodel it during natural stresses. We found that large “SPOTs” (structures positive for OMM) emerge during Toxoplasma gondii infection in mammalian cells. SPOTs mediated the depletion of the OMM proteins mitofusin 1 and 2, which restrict parasite growth. The formation of SPOTs depended on the parasite effector TgMAF1 and the host mitochondrial import receptor TOM70, which is required for optimal parasite proliferation. TOM70 enabled TgMAF1 to interact with the host OMM translocase SAM50. The ablation of SAM50 or the overexpression of an OMM-targeted protein promoted OMM remodeling independently of infection. Thus, Toxoplasma hijacks the formation of SPOTs, a cellular response to OMM stress, to promote its growth. |
| التعليقات: | Comment in: Cell Host Microbe. 2022 Mar 9;30(3):274-276. (PMID: 35271796) Comment in: Mol Cell. 2022 Mar 17;82(6):1086-1088. (PMID: 35303482) |
| معلومات مُعتمدة: | International ERC_ European Research Council |
| المشرفين على المادة: | 0 (Mitochondrial Membrane Transport Proteins) 0 (Mitochondrial Precursor Protein Import Complex Proteins) 0 (Mitochondrial Proteins) 0 (Protozoan Proteins) 0 (SAMM50 protein, human) 0 (TOMM70 protein, human) 0 (Tom70 protein, mouse) EC 3.6.1.- (GTP Phosphohydrolases) EC 3.6.1.- (MFN2 protein, human) EC 3.6.1.- (Mfn1 protein, mouse) EC 3.6.1.- (Mfn2 protein, mouse) EC 3.6.5.- (Mfn1 protein, human) |
| تواريخ الأحداث: | Date Created: 20220113 Date Completed: 20220128 Latest Revision: 20220411 |
| رمز التحديث: | 20221213 |
| DOI: | 10.1126/science.abi4343 |
| PMID: | 35025629 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1095-9203 |
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| DOI: | 10.1126/science.abi4343 |