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Functional Delivery of a Cytosolic tRNA into Mutant Mitochondria of Human Cells
Many maternally inherited and incurable neuromyopathies are caused by mutations in mitochondrial (mt) transfer RNA (tRNA) genes. Kinetoplastid protozoa, including Leishmania, have evolved specialized systems for importing nucleus-encoded tRNAs into mitochondria. We found that the Leishmania RNA impo...
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| Published in: | Science (American Association for the Advancement of Science) 2006-10, Vol.314 (5798), p.471-474 |
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| Main Authors: | , , , , |
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| Language: | English |
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| cites | cdi_FETCH-LOGICAL-c420t-c46df91c8f4ade3365283d3de71b2506285321af074e11ba4501cd8395c905eb3 |
| container_end_page | 474 |
| container_issue | 5798 |
| container_start_page | 471 |
| container_title | Science (American Association for the Advancement of Science) |
| container_volume | 314 |
| creator | Mahata, Bidesh Mukherjee, Saikat Mishra, Sumita Bandyopadhyay, Arun Adhya, Samit |
| description | Many maternally inherited and incurable neuromyopathies are caused by mutations in mitochondrial (mt) transfer RNA (tRNA) genes. Kinetoplastid protozoa, including Leishmania, have evolved specialized systems for importing nucleus-encoded tRNAs into mitochondria. We found that the Leishmania RNA import complex (RIC) could enter human cells by a caveolin-1-dependent pathway, where it induced import of endogenous cytosolic tRNAs, including tRNALys, and restored mitochondrial function in a cybrid harboring a mutant mt tRNALys (MT-TK) gene. The use of protein complexes to modulate mitochondrial function may help in the management of such genetic disorders. |
| doi_str_mv | 10.1126/science.1129754 |
| format | article |
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Kinetoplastid protozoa, including Leishmania, have evolved specialized systems for importing nucleus-encoded tRNAs into mitochondria. We found that the Leishmania RNA import complex (RIC) could enter human cells by a caveolin-1-dependent pathway, where it induced import of endogenous cytosolic tRNAs, including tRNALys, and restored mitochondrial function in a cybrid harboring a mutant mt tRNALys (MT-TK) gene. The use of protein complexes to modulate mitochondrial function may help in the management of such genetic disorders.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.1129754</identifier><identifier>PMID: 17053148</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Association for the Advancement of Science</publisher><subject>Animals ; Biological and medical sciences ; Caveolin 1 - metabolism ; Cell growth ; Cell Line, Tumor ; Cell lines ; Cell Proliferation ; Cell Respiration ; Cells, Cultured ; Cultured cells ; Cytosol - metabolism ; Electron Transport Complex IV - metabolism ; Endocytosis ; General aspects ; Genetic disorders ; Genetic engineering ; Genetic mutation ; Hep G2 cells ; Humans ; Imports ; Kearns-Sayre Syndrome - metabolism ; Leishmania ; Leishmania tropica ; Medical sciences ; MERRF Syndrome - metabolism ; Mitochondria ; Mitochondria - genetics ; Mitochondria - metabolism ; Mitochondrial Proteins - metabolism ; Mutation ; Neurological disorders ; Oxygen Consumption ; Protein Biosynthesis ; Proteins ; Protozoan Proteins - metabolism ; Reverse transcriptase polymerase chain reaction ; Ribonucleic acid ; RNA ; RNA, Transfer, Lys - genetics ; RNA, Transfer, Lys - metabolism ; RNA-Binding Proteins - metabolism ; Transfection ; Transfer RNA</subject><ispartof>Science (American Association for the Advancement of Science), 2006-10, Vol.314 (5798), p.471-474</ispartof><rights>Copyright 2006 American Association for the Advancement of Science</rights><rights>2006 INIST-CNRS</rights><rights>Copyright American Association for the Advancement of Science Oct 20, 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-c46df91c8f4ade3365283d3de71b2506285321af074e11ba4501cd8395c905eb3</citedby><cites>FETCH-LOGICAL-c420t-c46df91c8f4ade3365283d3de71b2506285321af074e11ba4501cd8395c905eb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2883,2884,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18236560$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17053148$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mahata, Bidesh</creatorcontrib><creatorcontrib>Mukherjee, Saikat</creatorcontrib><creatorcontrib>Mishra, Sumita</creatorcontrib><creatorcontrib>Bandyopadhyay, Arun</creatorcontrib><creatorcontrib>Adhya, Samit</creatorcontrib><title>Functional Delivery of a Cytosolic tRNA into Mutant Mitochondria of Human Cells</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Many maternally inherited and incurable neuromyopathies are caused by mutations in mitochondrial (mt) transfer RNA (tRNA) genes. Kinetoplastid protozoa, including Leishmania, have evolved specialized systems for importing nucleus-encoded tRNAs into mitochondria. We found that the Leishmania RNA import complex (RIC) could enter human cells by a caveolin-1-dependent pathway, where it induced import of endogenous cytosolic tRNAs, including tRNALys, and restored mitochondrial function in a cybrid harboring a mutant mt tRNALys (MT-TK) gene. The use of protein complexes to modulate mitochondrial function may help in the management of such genetic disorders.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Caveolin 1 - metabolism</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell lines</subject><subject>Cell Proliferation</subject><subject>Cell Respiration</subject><subject>Cells, Cultured</subject><subject>Cultured cells</subject><subject>Cytosol - metabolism</subject><subject>Electron Transport Complex IV - metabolism</subject><subject>Endocytosis</subject><subject>General aspects</subject><subject>Genetic disorders</subject><subject>Genetic engineering</subject><subject>Genetic mutation</subject><subject>Hep G2 cells</subject><subject>Humans</subject><subject>Imports</subject><subject>Kearns-Sayre Syndrome - metabolism</subject><subject>Leishmania</subject><subject>Leishmania tropica</subject><subject>Medical sciences</subject><subject>MERRF Syndrome - 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| ispartof | Science (American Association for the Advancement of Science), 2006-10, Vol.314 (5798), p.471-474 |
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| source | American Association for the Advancement of Science; Alma/SFX Local Collection |
| subjects | Animals Biological and medical sciences Caveolin 1 - metabolism Cell growth Cell Line, Tumor Cell lines Cell Proliferation Cell Respiration Cells, Cultured Cultured cells Cytosol - metabolism Electron Transport Complex IV - metabolism Endocytosis General aspects Genetic disorders Genetic engineering Genetic mutation Hep G2 cells Humans Imports Kearns-Sayre Syndrome - metabolism Leishmania Leishmania tropica Medical sciences MERRF Syndrome - metabolism Mitochondria Mitochondria - genetics Mitochondria - metabolism Mitochondrial Proteins - metabolism Mutation Neurological disorders Oxygen Consumption Protein Biosynthesis Proteins Protozoan Proteins - metabolism Reverse transcriptase polymerase chain reaction Ribonucleic acid RNA RNA, Transfer, Lys - genetics RNA, Transfer, Lys - metabolism RNA-Binding Proteins - metabolism Transfection Transfer RNA |
| title | Functional Delivery of a Cytosolic tRNA into Mutant Mitochondria of Human Cells |
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