DIC-1 over-expression enhances respiratory activity in Caenorhabditis elegans by promoting mitochondrial cristae formation
Deficiency of the Caenorhabditis elegans protein, DIC-1, located in the inner membrane of mitochondria produces an abnormal mitochondrial morphology. The mechanism by which DIC-1 controls the topology of the inner membrane was investigated by transiently over-expressing DIC-1 in C. elegans. Cryo-ele...
Gespeichert in:
| Veröffentlicht in: | Genes to cells : devoted to molecular & cellular mechanisms 2009-03, Vol.14 (3), p.319-327 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 327 |
|---|---|
| container_issue | 3 |
| container_start_page | 319 |
| container_title | Genes to cells : devoted to molecular & cellular mechanisms |
| container_volume | 14 |
| creator | Lee, Tae Hoon Mun, Ji Young Han, Sung Min Yoon, Gyesoon Han, Sung Sik Koo, Hyeon-Sook |
| description | Deficiency of the Caenorhabditis elegans protein, DIC-1, located in the inner membrane of mitochondria produces an abnormal mitochondrial morphology. The mechanism by which DIC-1 controls the topology of the inner membrane was investigated by transiently over-expressing DIC-1 in C. elegans. Cryo-electron microscopy showed that DIC-1 over-expression greatly increased the number and fractional area of mitochondrial cristae, suggesting that DIC-1 actively participates in cristae formation. These morphological changes were accompanied by increases in the oxygen consumption rate and ATP content of C. elegans worms, and decreases in reactive oxygen species (ROS) and sensitivity to paraquat. DIC-1 knockdown induced the opposite changes in ATP, ROS and paraquat-sensitivity. The ability of DIC-1 to increase cristae formation and secondarily, oxidative phosphorylation, suggests a potential use of this factor to control mitochondrial activity. |
| doi_str_mv | 10.1111/j.1365-2443.2008.01276.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67001080</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20450438</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4226-adb94c673192e6e0e7b63f0a330515af1ddfee3c585a83040eb29c25aba536013</originalsourceid><addsrcrecordid>eNqNkU1v1DAQhiMEoqXwF8AnbgljO87HgQMKtFSqxIH2bE2cya5XSbzY2bLh19dhV3AEXzyy33e-niRhHDIez4ddxmWhUpHnMhMAVQZclEV2fJZc_vl4vsaqSGtVlxfJqxB2AFwKUC-TC14LDiovL5Nfn2-blDP3SD6l495TCNZNjKYtToYCiw9763F2fmFoZvto54XZiTVIk_NbbDs728BooA1OgbUL23s3utlOGzba2ZmtmzpvcWDG2zAjsd75EedY5HXyosch0JvzfZU8XH-5b76md99ubptPd6nJhShS7No6N0UpY9NUEFDZFrIHlBIUV9jzruuJpFGVwkpCDtSK2giFLSpZxJGvkvenvLGzHwcKsx5tMDQMOJE7BF2UcTFQwT-FAnIFuayisDoJjXcheOr13tsR_aI56BWQ3umVg1456BWQ_g1IH6P17bnGoR2p-2s8E4mCjyfBTzvQ8t-J9c19s0bR_-7k79Fp3MSl64fvIq4BuKrjkEo-AajIqkQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>20450438</pqid></control><display><type>article</type><title>DIC-1 over-expression enhances respiratory activity in Caenorhabditis elegans by promoting mitochondrial cristae formation</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Access via Wiley Online Library</source><source>Wiley Free Content</source><source>Open Access Titles of Japan</source><creator>Lee, Tae Hoon ; Mun, Ji Young ; Han, Sung Min ; Yoon, Gyesoon ; Han, Sung Sik ; Koo, Hyeon-Sook</creator><creatorcontrib>Lee, Tae Hoon ; Mun, Ji Young ; Han, Sung Min ; Yoon, Gyesoon ; Han, Sung Sik ; Koo, Hyeon-Sook</creatorcontrib><description>Deficiency of the Caenorhabditis elegans protein, DIC-1, located in the inner membrane of mitochondria produces an abnormal mitochondrial morphology. The mechanism by which DIC-1 controls the topology of the inner membrane was investigated by transiently over-expressing DIC-1 in C. elegans. Cryo-electron microscopy showed that DIC-1 over-expression greatly increased the number and fractional area of mitochondrial cristae, suggesting that DIC-1 actively participates in cristae formation. These morphological changes were accompanied by increases in the oxygen consumption rate and ATP content of C. elegans worms, and decreases in reactive oxygen species (ROS) and sensitivity to paraquat. DIC-1 knockdown induced the opposite changes in ATP, ROS and paraquat-sensitivity. The ability of DIC-1 to increase cristae formation and secondarily, oxidative phosphorylation, suggests a potential use of this factor to control mitochondrial activity.</description><identifier>ISSN: 1356-9597</identifier><identifier>EISSN: 1365-2443</identifier><identifier>DOI: 10.1111/j.1365-2443.2008.01276.x</identifier><identifier>PMID: 19210547</identifier><language>eng</language><publisher>Malden, USA: Malden, USA : Blackwell Publishing Inc</publisher><subject>Animals ; Caenorhabditis elegans ; Caenorhabditis elegans - drug effects ; Caenorhabditis elegans - metabolism ; Caenorhabditis elegans Proteins - chemistry ; Caenorhabditis elegans Proteins - metabolism ; Cryoelectron Microscopy ; Drug Resistance ; Gene Knockdown Techniques ; Membrane Proteins - chemistry ; Membrane Proteins - metabolism ; Mitochondrial Membranes - metabolism ; Oxidative Phosphorylation ; Paraquat - pharmacology ; Protein Structure, Tertiary ; Reactive Oxygen Species - metabolism</subject><ispartof>Genes to cells : devoted to molecular & cellular mechanisms, 2009-03, Vol.14 (3), p.319-327</ispartof><rights>2009 The Authors. Journal compilation © 2009 by the Molecular Biology Society of Japan/Blackwell Publishing Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4226-adb94c673192e6e0e7b63f0a330515af1ddfee3c585a83040eb29c25aba536013</citedby><cites>FETCH-LOGICAL-c4226-adb94c673192e6e0e7b63f0a330515af1ddfee3c585a83040eb29c25aba536013</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2443.2008.01276.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2443.2008.01276.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,1433,27924,27925,45574,45575,46409,46833</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19210547$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Tae Hoon</creatorcontrib><creatorcontrib>Mun, Ji Young</creatorcontrib><creatorcontrib>Han, Sung Min</creatorcontrib><creatorcontrib>Yoon, Gyesoon</creatorcontrib><creatorcontrib>Han, Sung Sik</creatorcontrib><creatorcontrib>Koo, Hyeon-Sook</creatorcontrib><title>DIC-1 over-expression enhances respiratory activity in Caenorhabditis elegans by promoting mitochondrial cristae formation</title><title>Genes to cells : devoted to molecular & cellular mechanisms</title><addtitle>Genes Cells</addtitle><description>Deficiency of the Caenorhabditis elegans protein, DIC-1, located in the inner membrane of mitochondria produces an abnormal mitochondrial morphology. The mechanism by which DIC-1 controls the topology of the inner membrane was investigated by transiently over-expressing DIC-1 in C. elegans. Cryo-electron microscopy showed that DIC-1 over-expression greatly increased the number and fractional area of mitochondrial cristae, suggesting that DIC-1 actively participates in cristae formation. These morphological changes were accompanied by increases in the oxygen consumption rate and ATP content of C. elegans worms, and decreases in reactive oxygen species (ROS) and sensitivity to paraquat. DIC-1 knockdown induced the opposite changes in ATP, ROS and paraquat-sensitivity. The ability of DIC-1 to increase cristae formation and secondarily, oxidative phosphorylation, suggests a potential use of this factor to control mitochondrial activity.</description><subject>Animals</subject><subject>Caenorhabditis elegans</subject><subject>Caenorhabditis elegans - drug effects</subject><subject>Caenorhabditis elegans - metabolism</subject><subject>Caenorhabditis elegans Proteins - chemistry</subject><subject>Caenorhabditis elegans Proteins - metabolism</subject><subject>Cryoelectron Microscopy</subject><subject>Drug Resistance</subject><subject>Gene Knockdown Techniques</subject><subject>Membrane Proteins - chemistry</subject><subject>Membrane Proteins - metabolism</subject><subject>Mitochondrial Membranes - metabolism</subject><subject>Oxidative Phosphorylation</subject><subject>Paraquat - pharmacology</subject><subject>Protein Structure, Tertiary</subject><subject>Reactive Oxygen Species - metabolism</subject><issn>1356-9597</issn><issn>1365-2443</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhiMEoqXwF8AnbgljO87HgQMKtFSqxIH2bE2cya5XSbzY2bLh19dhV3AEXzyy33e-niRhHDIez4ddxmWhUpHnMhMAVQZclEV2fJZc_vl4vsaqSGtVlxfJqxB2AFwKUC-TC14LDiovL5Nfn2-blDP3SD6l495TCNZNjKYtToYCiw9763F2fmFoZvto54XZiTVIk_NbbDs728BooA1OgbUL23s3utlOGzba2ZmtmzpvcWDG2zAjsd75EedY5HXyosch0JvzfZU8XH-5b76md99ubptPd6nJhShS7No6N0UpY9NUEFDZFrIHlBIUV9jzruuJpFGVwkpCDtSK2giFLSpZxJGvkvenvLGzHwcKsx5tMDQMOJE7BF2UcTFQwT-FAnIFuayisDoJjXcheOr13tsR_aI56BWQ3umVg1456BWQ_g1IH6P17bnGoR2p-2s8E4mCjyfBTzvQ8t-J9c19s0bR_-7k79Fp3MSl64fvIq4BuKrjkEo-AajIqkQ</recordid><startdate>200903</startdate><enddate>200903</enddate><creator>Lee, Tae Hoon</creator><creator>Mun, Ji Young</creator><creator>Han, Sung Min</creator><creator>Yoon, Gyesoon</creator><creator>Han, Sung Sik</creator><creator>Koo, Hyeon-Sook</creator><general>Malden, USA : Blackwell Publishing Inc</general><general>Blackwell Publishing Inc</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>200903</creationdate><title>DIC-1 over-expression enhances respiratory activity in Caenorhabditis elegans by promoting mitochondrial cristae formation</title><author>Lee, Tae Hoon ; Mun, Ji Young ; Han, Sung Min ; Yoon, Gyesoon ; Han, Sung Sik ; Koo, Hyeon-Sook</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4226-adb94c673192e6e0e7b63f0a330515af1ddfee3c585a83040eb29c25aba536013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Caenorhabditis elegans</topic><topic>Caenorhabditis elegans - drug effects</topic><topic>Caenorhabditis elegans - metabolism</topic><topic>Caenorhabditis elegans Proteins - chemistry</topic><topic>Caenorhabditis elegans Proteins - metabolism</topic><topic>Cryoelectron Microscopy</topic><topic>Drug Resistance</topic><topic>Gene Knockdown Techniques</topic><topic>Membrane Proteins - chemistry</topic><topic>Membrane Proteins - metabolism</topic><topic>Mitochondrial Membranes - metabolism</topic><topic>Oxidative Phosphorylation</topic><topic>Paraquat - pharmacology</topic><topic>Protein Structure, Tertiary</topic><topic>Reactive Oxygen Species - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Tae Hoon</creatorcontrib><creatorcontrib>Mun, Ji Young</creatorcontrib><creatorcontrib>Han, Sung Min</creatorcontrib><creatorcontrib>Yoon, Gyesoon</creatorcontrib><creatorcontrib>Han, Sung Sik</creatorcontrib><creatorcontrib>Koo, Hyeon-Sook</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genes to cells : devoted to molecular & cellular mechanisms</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Tae Hoon</au><au>Mun, Ji Young</au><au>Han, Sung Min</au><au>Yoon, Gyesoon</au><au>Han, Sung Sik</au><au>Koo, Hyeon-Sook</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DIC-1 over-expression enhances respiratory activity in Caenorhabditis elegans by promoting mitochondrial cristae formation</atitle><jtitle>Genes to cells : devoted to molecular & cellular mechanisms</jtitle><addtitle>Genes Cells</addtitle><date>2009-03</date><risdate>2009</risdate><volume>14</volume><issue>3</issue><spage>319</spage><epage>327</epage><pages>319-327</pages><issn>1356-9597</issn><eissn>1365-2443</eissn><abstract>Deficiency of the Caenorhabditis elegans protein, DIC-1, located in the inner membrane of mitochondria produces an abnormal mitochondrial morphology. The mechanism by which DIC-1 controls the topology of the inner membrane was investigated by transiently over-expressing DIC-1 in C. elegans. Cryo-electron microscopy showed that DIC-1 over-expression greatly increased the number and fractional area of mitochondrial cristae, suggesting that DIC-1 actively participates in cristae formation. These morphological changes were accompanied by increases in the oxygen consumption rate and ATP content of C. elegans worms, and decreases in reactive oxygen species (ROS) and sensitivity to paraquat. DIC-1 knockdown induced the opposite changes in ATP, ROS and paraquat-sensitivity. The ability of DIC-1 to increase cristae formation and secondarily, oxidative phosphorylation, suggests a potential use of this factor to control mitochondrial activity.</abstract><cop>Malden, USA</cop><pub>Malden, USA : Blackwell Publishing Inc</pub><pmid>19210547</pmid><doi>10.1111/j.1365-2443.2008.01276.x</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1356-9597 |
| ispartof | Genes to cells : devoted to molecular & cellular mechanisms, 2009-03, Vol.14 (3), p.319-327 |
| issn | 1356-9597 1365-2443 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67001080 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Access via Wiley Online Library; Wiley Free Content; Open Access Titles of Japan |
| subjects | Animals Caenorhabditis elegans Caenorhabditis elegans - drug effects Caenorhabditis elegans - metabolism Caenorhabditis elegans Proteins - chemistry Caenorhabditis elegans Proteins - metabolism Cryoelectron Microscopy Drug Resistance Gene Knockdown Techniques Membrane Proteins - chemistry Membrane Proteins - metabolism Mitochondrial Membranes - metabolism Oxidative Phosphorylation Paraquat - pharmacology Protein Structure, Tertiary Reactive Oxygen Species - metabolism |
| title | DIC-1 over-expression enhances respiratory activity in Caenorhabditis elegans by promoting mitochondrial cristae formation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-04T02%3A44%3A33IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=DIC-1%20over-expression%20enhances%20respiratory%20activity%20in%20Caenorhabditis%20elegans%20by%20promoting%20mitochondrial%20cristae%20formation&rft.jtitle=Genes%20to%20cells%20:%20devoted%20to%20molecular%20&%20cellular%20mechanisms&rft.au=Lee,%20Tae%20Hoon&rft.date=2009-03&rft.volume=14&rft.issue=3&rft.spage=319&rft.epage=327&rft.pages=319-327&rft.issn=1356-9597&rft.eissn=1365-2443&rft_id=info:doi/10.1111/j.1365-2443.2008.01276.x&rft_dat=%3Cproquest_cross%3E20450438%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=20450438&rft_id=info:pmid/19210547&rfr_iscdi=true |