Sub-mitochondrial localization of the genetic-tagged mitochondrial intermembrane space-bridging components Mic19, Mic60 and Sam50

Sastri, Mira; Darshi, Manjula; Mackey, Mason; Ramachandra, Ranjan; Ju, Saeyeon; Phan, Sébastien; Adams, Stephen; Stein, Kathryn R.; Douglas, Chris; Kim, Jiwan John; Ellisman, Mark H.; Taylor, Susan S.; Perkins, Guy

doi:10.1242/jcs.201400

Cited by 29 publications

(35 citation statements)

References 91 publications

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“…Subunit MIC10 plays a central role in the yeast MICOS system (31), and MIC10 oligomerization induces MOM bending at CJs (17). Electron tomography analysis revealed that MIC19 and MIC60 were enriched inside cristae and localized at CJs (346). Moreover, the latter study provided evidence that MIC19 interacted with subunit IV of CIV.…”

Section: Fig 7 Key Mechanisms That Govern Dynamic Changes In Mitochmentioning

confidence: 77%

Mitochondrial Morphofunction in Mammalian Cells

Bulthuis

Adjobo‐Hermans

Willems

et al. 2019

Antioxidants & Redox Signaling

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Significance: In addition to their classical role in cellular ATP production, mitochondria are of key relevance in various (patho)physiological mechanisms including second messenger signaling, neuro-transduction, immune responses and death induction. Recent Advances: Within cells, mitochondria are motile and display temporal changes in internal and external structure (''mitochondrial dynamics''). During the last decade, substantial empirical and in silico evidence was presented demonstrating that mitochondrial dynamics impacts on mitochondrial function and vice versa. Critical Issues: However, a comprehensive and quantitative understanding of the bidirectional links between mitochondrial external shape, internal structure and function (''morphofunction'') is still lacking. The latter particularly hampers our understanding of the functional properties and behavior of individual mitochondrial within single living cells. Future Directions: In this review we discuss the concept of mitochondrial morphofunction in mammalian cells, primarily using experimental evidence obtained within the last decade. The topic is introduced by briefly presenting the central role of mitochondria in cell physiology and the importance of the mitochondrial electron transport chain (ETC) therein. Next, we summarize in detail how mitochondrial (ultra)structure is controlled and discuss empirical evidence regarding the equivalence of mitochondrial (ultra)structure and function. Finally, we provide a brief summary of how mitochondrial morphofunction can be quantified at the level of single cells and mitochondria, how mitochondrial ultrastructure/volume impacts on mitochondrial bioreactions and intramitochondrial protein diffusion, and how mitochondrial morphofunction can be targeted by small molecules.

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Section: Fig 7 Key Mechanisms That Govern Dynamic Changes In Mitochmentioning

confidence: 77%

Mitochondrial Morphofunction in Mammalian Cells

Bulthuis

Adjobo‐Hermans

Willems

et al. 2019

Antioxidants & Redox Signaling

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“…Another intriguing possibility is that the synthesis of PE by Psd1p in the IM is somehow directly coupled to the incorporation of this lipid into partially or fully assembled complex III. Recently, a subunit of complex IV was found to associate with the MICOS subunit, Mic19, in mammalian cells by EM tomography and immunoprecipitation (44). As the MICOS complex was suggested to work in concert with Ups2p to regulate mitochondrial PS/PE metabolism in yeast (26), potentially, contact sites between the OM and IM could facilitate the transport of ER-derived PE to complex IV more directly than it can to complex III.…”

Section: Discussionmentioning

confidence: 99%

Phosphatidylethanolamine made in the inner mitochondrial membrane is essential for yeast cytochromebc₁complex function

Calzada

Claypool

2018

Preprint

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Of the four separate PE biosynthetic pathways in eukaryotes, one occurs in the mitochondrial inner membrane (IM) and is executed by phosphatidylserine decarboxylase (Psd1p). Deletion of Psd1, which is lethal in mice, compromises mitochondrial function. We hypothesize that this reflects inefficient import of non-mitochondrial PE into the IM. To test this, we re-wired PE metabolism in yeast by re-directing Psd1p to the outer mitochondrial membrane or the endomembrane system. Our biochemical and functional analyses identified the IMS as the greatest barrier for PE import and demonstrated that PE synthesis in the IM is critical for cytochrome bc1 complex (III) function. Importantly, mutations predicted to disrupt a conserved PE-binding site in the complex III subunit, Qcr7p, impaired complex III activity similar to PSD1 deletion. Collectively, these data demonstrate that PE made in the IM by Psd1p is critical to support the intrinsic functionality of complex III and establish one likely mechanism.

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“…In mammalian cells, MICOS and SAM form a stable supercomplex that was termed mitochondrial intermembrane space bridging complex (MIB) (Fig. ) . These interactions support the import of a subset of mitochondrial proteins, and, importantly, they establish contact sites between the two mitochondrial membranes .…”

Section: The Mitochondrial Contact Site and Cristae Organizing Systemmentioning

confidence: 99%

Shaping the mitochondrial inner membrane in health and disease

et al. 2020

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Colina-Tenorio L, Horten P, Pfanner N, Rampelt H (University of Freiburg, Freiburg, Germany). Shaping the mitochondrial inner membrane in health and disease (Review Symposium). J Intern Med 2020; 287: 645-664.Mitochondria play central roles in cellular energetics, metabolism and signalling. Efficient respiration, mitochondrial quality control, apoptosis and inheritance of mitochondrial DNA depend on the proper architecture of the mitochondrial membranes and a dynamic remodelling of inner membrane cristae. Defects in mitochondrial architecture can result in severe human diseases affecting predominantly the nervous system and the heart. Inner membrane morphology is generated and maintained in particular by the mitochondrial contact site and cristae organizing system (MICOS), the F 1 F o -ATP synthase, the fusion protein OPA1/Mgm1 and the nonbilayer-forming phospholipids cardiolipin and phosphatidylethanolamine. These protein complexes and phospholipids are embedded in a network of functional interactions. They communicate with each other and additional factors, enabling them to balance different aspects of cristae biogenesis and to dynamically remodel the inner mitochondrial membrane. Genetic alterations disturbing these membrane-shaping factors can lead to human pathologies including fatal encephalopathy, dominant optic atrophy, Leigh syndrome, Parkinson's disease and Barth syndrome.

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Sub-mitochondrial localization of the genetic-tagged mitochondrial intermembrane space-bridging components Mic19, Mic60 and Sam50

Cited by 29 publications

References 91 publications

Mitochondrial Morphofunction in Mammalian Cells

Mitochondrial Morphofunction in Mammalian Cells

Phosphatidylethanolamine made in the inner mitochondrial membrane is essential for yeast cytochromebc₁complex function

Shaping the mitochondrial inner membrane in health and disease

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Sub-mitochondrial localization of the genetic-tagged mitochondrial intermembrane space-bridging components Mic19, Mic60 and Sam50

Cited by 29 publications

References 91 publications

Mitochondrial Morphofunction in Mammalian Cells

Mitochondrial Morphofunction in Mammalian Cells

Phosphatidylethanolamine made in the inner mitochondrial membrane is essential for yeast cytochromebc1complex function

Shaping the mitochondrial inner membrane in health and disease

Contact Info

Product

Resources

About

Phosphatidylethanolamine made in the inner mitochondrial membrane is essential for yeast cytochromebc₁complex function