دورية أكاديمية
أعرض في EDS

Lysosomes drive the piecemeal removal of mitochondrial inner membrane.

التفاصيل البيبلوغرافية
العنوان: Lysosomes drive the piecemeal removal of mitochondrial inner membrane.
المؤلفون: Prashar A; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada.; NHLBI, NIH, Bethesda, MD, USA., Bussi C; Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.; School of Biological Sciences, Nanyang Technical University, Singapore, Singapore., Fearns A; Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK., Capurro MI; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada., Gao X; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada., Sesaki H; Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, MD, USA., Gutierrez MG; Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK., Jones NL; Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada. Nicola.jones@sickkids.ca.; Division of Gastroenterology, Hepatology and Nutrition, The Hospital for Sick Children, Toronto, Ontario, Canada. Nicola.jones@sickkids.ca.; Departments of Paediatrics and Physiology, University of Toronto, Toronto, Ontario, Canada. Nicola.jones@sickkids.ca.
المصدر: Nature [Nature] 2024 Aug; Vol. 632 (8027), pp. 1110-1117. Date of Electronic Publication: 2024 Aug 21.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 0410462 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-4687 (Electronic) Linking ISSN: 00280836 NLM ISO Abbreviation: Nature Subsets: MEDLINE
أسماء مطبوعة: Publication: Basingstoke : Nature Publishing Group
Original Publication: London, Macmillan Journals ltd.
مواضيع طبية MeSH: Lysosomes*/metabolism , Mitochondria*/metabolism , Mitochondria*/pathology , Mitochondrial Membranes*/chemistry , Mitochondrial Membranes*/metabolism, Animals ; Humans ; Mice ; Autophagy ; Calcium/metabolism ; Cytosol/metabolism ; Homeostasis ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Transient Receptor Potential Channels/metabolism ; Voltage-Dependent Anion Channel 1/metabolism ; Cell Compartmentation ; Mitochondrial Dynamics
مستخلص: Mitochondrial membranes define distinct structural and functional compartments. Cristae of the inner mitochondrial membrane (IMM) function as independent bioenergetic units that undergo rapid and transient remodelling, but the significance of this compartmentalized organization is unknown 1 . Using super-resolution microscopy, here we show that cytosolic IMM vesicles, devoid of outer mitochondrial membrane or mitochondrial matrix, are formed during resting state. These vesicles derived from the IMM (VDIMs) are formed by IMM herniation through pores formed by voltage-dependent anion channel 1 in the outer mitochondrial membrane. Live-cell imaging showed that lysosomes in proximity to mitochondria engulfed the herniating IMM and, aided by the endosomal sorting complex required for transport machinery, led to the formation of VDIMs in a microautophagy-like process, sparing the remainder of the organelle. VDIM formation was enhanced in mitochondria undergoing oxidative stress, suggesting their potential role in maintenance of mitochondrial function. Furthermore, the formation of VDIMs required calcium release by the reactive oxygen species-activated, lysosomal calcium channel, transient receptor potential mucolipin 1, showing an interorganelle communication pathway for maintenance of mitochondrial homeostasis. Thus, IMM compartmentalization could allow for the selective removal of damaged IMM sections via VDIMs, which should protect mitochondria from localized injury. Our findings show a new pathway of intramitochondrial quality control.
(© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)
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معلومات مُعتمدة: United Kingdom WT_ Wellcome Trust; CC2081 United Kingdom ARC_ Arthritis Research UK; FC001092 United Kingdom ARC_ Arthritis Research UK; R35 GM144103 United States GM NIGMS NIH HHS
المشرفين على المادة: SY7Q814VUP (Calcium)
0 (MCOLN1 protein, human)
0 (Reactive Oxygen Species)
0 (Transient Receptor Potential Channels)
EC 1.6.- (Voltage-Dependent Anion Channel 1)
0 (Mcoln1 protein, mouse)
تواريخ الأحداث: Date Created: 20240821 Date Completed: 20240829 Latest Revision: 20240928
رمز التحديث: 20240928
مُعرف محوري في PubMed: PMC7616637
DOI: 10.1038/s41586-024-07835-w
PMID: 39169179
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-4687
DOI:10.1038/s41586-024-07835-w