Dynamics of Human Mitochondrial Complex I Assembly: Implications for Neurodegenerative Diseases
Identifieur interne : 000090 ( Pmc/Checkpoint ); précédent : 000089; suivant : 000091Dynamics of Human Mitochondrial Complex I Assembly: Implications for Neurodegenerative Diseases
Auteurs : Gabriele Giachin ; Romain Bouverot ; Samira Acajjaoui ; Serena Pantalone ; Montserrat Soler-L PezSource :
- Frontiers in Molecular Biosciences [ 2296-889X ] ; 2016.
Abstract
Neurons are extremely energy demanding cells and highly dependent on the mitochondrial oxidative phosphorylation (OXPHOS) system. Mitochondria generate the energetic potential via the respiratory complexes I to IV, which constitute the electron transport chain (ETC), together with complex V. These redox reactions release energy in the form of ATP and also generate reactive oxygen species (ROS) that are involved in cell signaling but can eventually lead to oxidative stress. Complex I (CI or NADH:ubiquinone oxidoreductase) is the largest ETC enzyme, containing 44 subunits and the main contributor to ROS production. In recent years, the structure of the CI has become available and has provided new insights into CI assembly. A number of chaperones have been identified in the assembly and stability of the mature holo-CI, although they are not part of its final structure. Interestingly, CI dysfunction is the most common OXPHOS disorder in humans and defects in the CI assembly process are often observed. However, the dynamics of the events leading to CI biogenesis remain elusive, which precludes our understanding of how ETC malfunctioning affects neuronal integrity. Here, we review the current knowledge of the structural features of CI and its assembly factors and the potential role of CI misassembly in human disorders such as Complex I Deficiencies or Alzheimer's and Parkinson's diseases.
Url:
DOI: 10.3389/fmolb.2016.00043
PubMed: 27597947
PubMed Central: 4992684
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Dynamics of Human Mitochondrial Complex I Assembly: Implications for Neurodegenerative Diseases</title><author><name sortKey="Giachin, Gabriele" sort="Giachin, Gabriele" uniqKey="Giachin G" first="Gabriele" last="Giachin">Gabriele Giachin</name></author><author><name sortKey="Bouverot, Romain" sort="Bouverot, Romain" uniqKey="Bouverot R" first="Romain" last="Bouverot">Romain Bouverot</name></author><author><name sortKey="Acajjaoui, Samira" sort="Acajjaoui, Samira" uniqKey="Acajjaoui S" first="Samira" last="Acajjaoui">Samira Acajjaoui</name></author><author><name sortKey="Pantalone, Serena" sort="Pantalone, Serena" uniqKey="Pantalone S" first="Serena" last="Pantalone">Serena Pantalone</name></author><author><name sortKey="Soler L Pez, Montserrat" sort="Soler L Pez, Montserrat" uniqKey="Soler L Pez M" first="Montserrat" last="Soler-L Pez">Montserrat Soler-L Pez</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">27597947</idno><idno type="pmc">4992684</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4992684</idno><idno type="RBID">PMC:4992684</idno><idno type="doi">10.3389/fmolb.2016.00043</idno><date when="2016">2016</date><idno type="wicri:Area/Pmc/Corpus">000941</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000941</idno><idno type="wicri:Area/Pmc/Curation">000937</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000937</idno><idno type="wicri:Area/Pmc/Checkpoint">000090</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000090</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Dynamics of Human Mitochondrial Complex I Assembly: Implications for Neurodegenerative Diseases</title><author><name sortKey="Giachin, Gabriele" sort="Giachin, Gabriele" uniqKey="Giachin G" first="Gabriele" last="Giachin">Gabriele Giachin</name></author><author><name sortKey="Bouverot, Romain" sort="Bouverot, Romain" uniqKey="Bouverot R" first="Romain" last="Bouverot">Romain Bouverot</name></author><author><name sortKey="Acajjaoui, Samira" sort="Acajjaoui, Samira" uniqKey="Acajjaoui S" first="Samira" last="Acajjaoui">Samira Acajjaoui</name></author><author><name sortKey="Pantalone, Serena" sort="Pantalone, Serena" uniqKey="Pantalone S" first="Serena" last="Pantalone">Serena Pantalone</name></author><author><name sortKey="Soler L Pez, Montserrat" sort="Soler L Pez, Montserrat" uniqKey="Soler L Pez M" first="Montserrat" last="Soler-L Pez">Montserrat Soler-L Pez</name></author></analytic><series><title level="j">Frontiers in Molecular Biosciences</title><idno type="eISSN">2296-889X</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Neurons are extremely energy demanding cells and highly dependent on the mitochondrial oxidative phosphorylation (OXPHOS) system. Mitochondria generate the energetic potential via the respiratory complexes I to IV, which constitute the electron transport chain (ETC), together with complex V. These redox reactions release energy in the form of ATP and also generate reactive oxygen species (ROS) that are involved in cell signaling but can eventually lead to oxidative stress. Complex I (CI or NADH:ubiquinone oxidoreductase) is the largest ETC enzyme, containing 44 subunits and the main contributor to ROS production. In recent years, the structure of the CI has become available and has provided new insights into CI assembly. A number of chaperones have been identified in the assembly and stability of the mature holo-CI, although they are not part of its final structure. Interestingly, CI dysfunction is the most common OXPHOS disorder in humans and defects in the CI assembly process are often observed. However, the dynamics of the events leading to CI biogenesis remain elusive, which precludes our understanding of how ETC malfunctioning affects neuronal integrity. Here, we review the current knowledge of the structural features of CI and its assembly factors and the potential role of CI misassembly in human disorders such as Complex I Deficiencies or Alzheimer's and Parkinson's diseases.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Aksenov, M Y" uniqKey="Aksenov M">M. Y. Aksenov</name></author><author><name sortKey="Tucker, H M" uniqKey="Tucker H">H. M. Tucker</name></author><author><name sortKey="Nair, P" uniqKey="Nair P">P. Nair</name></author><author><name sortKey="Aksenova, M V" uniqKey="Aksenova M">M. V. Aksenova</name></author><author><name sortKey="Butterfield, D A" uniqKey="Butterfield D">D. A. Butterfield</name></author><author><name sortKey="Estus, S" uniqKey="Estus S">S. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Mol Biosci</journal-id><journal-id journal-id-type="iso-abbrev">Front Mol Biosci</journal-id><journal-id journal-id-type="publisher-id">Front. Mol. Biosci.</journal-id><journal-title-group><journal-title>Frontiers in Molecular Biosciences</journal-title></journal-title-group><issn pub-type="epub">2296-889X</issn><publisher><publisher-name>Frontiers Media S.A.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">27597947</article-id><article-id pub-id-type="pmc">4992684</article-id><article-id pub-id-type="doi">10.3389/fmolb.2016.00043</article-id><article-categories><subj-group subj-group-type="heading"><subject>Molecular Biosciences</subject><subj-group><subject>Review</subject></subj-group></subj-group></article-categories><title-group><article-title>Dynamics of Human Mitochondrial Complex I Assembly: Implications for Neurodegenerative Diseases</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Giachin</surname><given-names>Gabriele</given-names></name><uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/272729/overview"></uri></contrib><contrib contrib-type="author"><name><surname>Bouverot</surname><given-names>Romain</given-names></name></contrib><contrib contrib-type="author"><name><surname>Acajjaoui</surname><given-names>Samira</given-names></name></contrib><contrib contrib-type="author"><name><surname>Pantalone</surname><given-names>Serena</given-names></name></contrib><contrib contrib-type="author"><name><surname>Soler-López</surname><given-names>Montserrat</given-names></name><xref ref-type="author-notes" rid="fn001"><sup>*</sup></xref><uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/290725/overview"></uri></contrib></contrib-group><aff><institution>Structural Biology Group, European Synchrotron Radiation Facility</institution><country>Grenoble, France</country></aff><author-notes><fn fn-type="edited-by"><p>Edited by: Luca Mollica, Italian Institute of Technology, Italy</p></fn><fn fn-type="edited-by"><p>Reviewed by: Revati Wani, Pfizer, USA; Trevor P. Creamer, University of Kentucky, USA</p></fn><corresp id="fn001">*Correspondence: Montserrat Soler-López <email xlink:type="simple">montserrat.soler-lopez@esrf.fr</email></corresp><fn fn-type="other" id="fn002"><p>This article was submitted to Molecular Recognition, a section of the journal Frontiers in Molecular Biosciences</p></fn></author-notes><pub-date pub-type="epub"><day>22</day><month>8</month><year>2016</year></pub-date><pub-date pub-type="collection"><year>2016</year></pub-date><volume>3</volume><elocation-id>43</elocation-id><history><date date-type="received"><day>07</day><month>6</month><year>2016</year></date><date date-type="accepted"><day>02</day><month>8</month><year>2016</year></date></history><permissions><copyright-statement>Copyright © 2016 Giachin, Bouverot, Acajjaoui, Pantalone and Soler-López.</copyright-statement><copyright-year>2016</copyright-year><copyright-holder>Giachin, Bouverot, Acajjaoui, Pantalone and Soler-López</copyright-holder><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p></license></permissions><abstract><p>Neurons are extremely energy demanding cells and highly dependent on the mitochondrial oxidative phosphorylation (OXPHOS) system. Mitochondria generate the energetic potential via the respiratory complexes I to IV, which constitute the electron transport chain (ETC), together with complex V. These redox reactions release energy in the form of ATP and also generate reactive oxygen species (ROS) that are involved in cell signaling but can eventually lead to oxidative stress. Complex I (CI or NADH:ubiquinone oxidoreductase) is the largest ETC enzyme, containing 44 subunits and the main contributor to ROS production. In recent years, the structure of the CI has become available and has provided new insights into CI assembly. A number of chaperones have been identified in the assembly and stability of the mature holo-CI, although they are not part of its final structure. Interestingly, CI dysfunction is the most common OXPHOS disorder in humans and defects in the CI assembly process are often observed. However, the dynamics of the events leading to CI biogenesis remain elusive, which precludes our understanding of how ETC malfunctioning affects neuronal integrity. Here, we review the current knowledge of the structural features of CI and its assembly factors and the potential role of CI misassembly in human disorders such as Complex I Deficiencies or Alzheimer's and Parkinson's diseases.</p></abstract><kwd-group><kwd>complex I</kwd><kwd>MCIA</kwd><kwd>assembly factors</kwd><kwd>mitochondrial dysfunction</kwd><kwd>neurodegeneration</kwd><kwd>Alzheimer's disease</kwd><kwd>Parkinson's disease</kwd></kwd-group><funding-group><award-group><funding-source id="cn001">European Synchrotron Radiation Facility<named-content content-type="fundref-id">10.13039/501100001671</named-content></funding-source></award-group></funding-group><counts><fig-count count="5"></fig-count><table-count count="2"></table-count><equation-count count="0"></equation-count><ref-count count="192"></ref-count><page-count count="20"></page-count><word-count count="15576"></word-count></counts></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Acajjaoui, Samira" sort="Acajjaoui, Samira" uniqKey="Acajjaoui S" first="Samira" last="Acajjaoui">Samira Acajjaoui</name><name sortKey="Bouverot, Romain" sort="Bouverot, Romain" uniqKey="Bouverot R" first="Romain" last="Bouverot">Romain Bouverot</name><name sortKey="Giachin, Gabriele" sort="Giachin, Gabriele" uniqKey="Giachin G" first="Gabriele" last="Giachin">Gabriele Giachin</name><name sortKey="Pantalone, Serena" sort="Pantalone, Serena" uniqKey="Pantalone S" first="Serena" last="Pantalone">Serena Pantalone</name><name sortKey="Soler L Pez, Montserrat" sort="Soler L Pez, Montserrat" uniqKey="Soler L Pez M" first="Montserrat" last="Soler-L Pez">Montserrat Soler-L Pez</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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