A conditional knockout rat resource of mitochondrial protein-coding genes via a DdCBE-induced premature stop codon
Hundreds of pathogenic variants of mitochondrial DNA (mtDNA) have been reported to cause mitochondrial diseases, which still lack effective treatments. It is a huge challenge to install these mutations one by one. We repurposed the DddA-derived cytosine base editor to incorporate a premature stop co...
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| Veröffentlicht in: | Science advances 2023-04, Vol.9 (15), p.eadf2695-eadf2695 |
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| creator | Tan, Lei Qi, Xiaolong Kong, Weining Jin, Jiachuan Lu, Dan Zhang, Xu Wang, Yue Wang, Siting Dong, Wei Shi, Xudong Chen, Wei Wang, Jianying Li, Keru Xie, Yuan Gao, Lijuan Guan, Feifei Gao, Kai Li, Chaojun Wang, Cheng Hu, Zhibin Zhang, Lianfeng Guo, Xuejiang Shen, Bin Ma, Yuanwu |
| description | Hundreds of pathogenic variants of mitochondrial DNA (mtDNA) have been reported to cause mitochondrial diseases, which still lack effective treatments. It is a huge challenge to install these mutations one by one. We repurposed the DddA-derived cytosine base editor to incorporate a premature stop codon in the mtProtein-coding genes to ablate mitochondrial proteins encoded in the mtDNA (mtProteins) instead of installing pathogenic variants and generated a library of both cell and rat resources with mtProtein depletion. In vitro, we depleted 12 of 13 mtProtein-coding genes with high efficiency and specificity, resulting in decreased mtProtein levels and impaired oxidative phosphorylation. Moreover, we generated six conditional knockout rat strains to ablate mtProteins using
system. Mitochondrially encoded ATP synthase membrane subunit 8 and NADH:ubiquinone oxidoreductase core subunit 1 were specifically depleted in heart cells or neurons, resulting in heart failure or abnormal brain development. Our work provides cell and rat resources for studying the function of mtProtein-coding genes and therapeutic strategies. |
| doi_str_mv | 10.1126/sciadv.adf2695 |
| format | Article |
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system. Mitochondrially encoded ATP synthase membrane subunit 8 and NADH:ubiquinone oxidoreductase core subunit 1 were specifically depleted in heart cells or neurons, resulting in heart failure or abnormal brain development. Our work provides cell and rat resources for studying the function of mtProtein-coding genes and therapeutic strategies.</description><identifier>ISSN: 2375-2548</identifier><identifier>EISSN: 2375-2548</identifier><identifier>DOI: 10.1126/sciadv.adf2695</identifier><identifier>PMID: 37058569</identifier><language>eng</language><publisher>United States: American Association for the Advancement of Science</publisher><subject>Animals ; Base Sequence ; Biomedicine and Life Sciences ; Codon, Nonsense ; Diseases and Disorders ; DNA, Mitochondrial - genetics ; DNA, Mitochondrial - metabolism ; Genetics ; Mitochondria - genetics ; Mitochondria - metabolism ; Mutation ; Rats ; Research Resource ; SciAdv r-resources</subject><ispartof>Science advances, 2023-04, Vol.9 (15), p.eadf2695-eadf2695</ispartof><rights>Copyright © 2023 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC). 2023 The Authors</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-f2946a651283386a5137906410eca30d6d1a6f24dc0d566dce64e2564fd6e7273</citedby><cites>FETCH-LOGICAL-c391t-f2946a651283386a5137906410eca30d6d1a6f24dc0d566dce64e2564fd6e7273</cites><orcidid>0000-0002-4038-0381 ; 0000-0002-8277-5234 ; 0000-0002-8946-8448 ; 0000-0002-5774-2924 ; 0000-0001-9474-7321 ; 0000-0002-0475-5705 ; 0000-0002-6183-2666 ; 0000-0002-6170-5704 ; 0000-0002-5204-2574 ; 0000-0002-8193-9276 ; 0000-0001-5084-6731 ; 0000-0002-1882-1777 ; 0000-0002-8651-2626</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10104465/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10104465/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37058569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tan, Lei</creatorcontrib><creatorcontrib>Qi, Xiaolong</creatorcontrib><creatorcontrib>Kong, Weining</creatorcontrib><creatorcontrib>Jin, Jiachuan</creatorcontrib><creatorcontrib>Lu, Dan</creatorcontrib><creatorcontrib>Zhang, Xu</creatorcontrib><creatorcontrib>Wang, Yue</creatorcontrib><creatorcontrib>Wang, Siting</creatorcontrib><creatorcontrib>Dong, Wei</creatorcontrib><creatorcontrib>Shi, Xudong</creatorcontrib><creatorcontrib>Chen, Wei</creatorcontrib><creatorcontrib>Wang, Jianying</creatorcontrib><creatorcontrib>Li, Keru</creatorcontrib><creatorcontrib>Xie, Yuan</creatorcontrib><creatorcontrib>Gao, Lijuan</creatorcontrib><creatorcontrib>Guan, Feifei</creatorcontrib><creatorcontrib>Gao, Kai</creatorcontrib><creatorcontrib>Li, Chaojun</creatorcontrib><creatorcontrib>Wang, Cheng</creatorcontrib><creatorcontrib>Hu, Zhibin</creatorcontrib><creatorcontrib>Zhang, Lianfeng</creatorcontrib><creatorcontrib>Guo, Xuejiang</creatorcontrib><creatorcontrib>Shen, Bin</creatorcontrib><creatorcontrib>Ma, Yuanwu</creatorcontrib><title>A conditional knockout rat resource of mitochondrial protein-coding genes via a DdCBE-induced premature stop codon</title><title>Science advances</title><addtitle>Sci Adv</addtitle><description>Hundreds of pathogenic variants of mitochondrial DNA (mtDNA) have been reported to cause mitochondrial diseases, which still lack effective treatments. It is a huge challenge to install these mutations one by one. We repurposed the DddA-derived cytosine base editor to incorporate a premature stop codon in the mtProtein-coding genes to ablate mitochondrial proteins encoded in the mtDNA (mtProteins) instead of installing pathogenic variants and generated a library of both cell and rat resources with mtProtein depletion. In vitro, we depleted 12 of 13 mtProtein-coding genes with high efficiency and specificity, resulting in decreased mtProtein levels and impaired oxidative phosphorylation. Moreover, we generated six conditional knockout rat strains to ablate mtProteins using
system. Mitochondrially encoded ATP synthase membrane subunit 8 and NADH:ubiquinone oxidoreductase core subunit 1 were specifically depleted in heart cells or neurons, resulting in heart failure or abnormal brain development. 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system. Mitochondrially encoded ATP synthase membrane subunit 8 and NADH:ubiquinone oxidoreductase core subunit 1 were specifically depleted in heart cells or neurons, resulting in heart failure or abnormal brain development. Our work provides cell and rat resources for studying the function of mtProtein-coding genes and therapeutic strategies.</abstract><cop>United States</cop><pub>American Association for the Advancement of Science</pub><pmid>37058569</pmid><doi>10.1126/sciadv.adf2695</doi><orcidid>https://orcid.org/0000-0002-4038-0381</orcidid><orcidid>https://orcid.org/0000-0002-8277-5234</orcidid><orcidid>https://orcid.org/0000-0002-8946-8448</orcidid><orcidid>https://orcid.org/0000-0002-5774-2924</orcidid><orcidid>https://orcid.org/0000-0001-9474-7321</orcidid><orcidid>https://orcid.org/0000-0002-0475-5705</orcidid><orcidid>https://orcid.org/0000-0002-6183-2666</orcidid><orcidid>https://orcid.org/0000-0002-6170-5704</orcidid><orcidid>https://orcid.org/0000-0002-5204-2574</orcidid><orcidid>https://orcid.org/0000-0002-8193-9276</orcidid><orcidid>https://orcid.org/0000-0001-5084-6731</orcidid><orcidid>https://orcid.org/0000-0002-1882-1777</orcidid><orcidid>https://orcid.org/0000-0002-8651-2626</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Base Sequence Biomedicine and Life Sciences Codon, Nonsense Diseases and Disorders DNA, Mitochondrial - genetics DNA, Mitochondrial - metabolism Genetics Mitochondria - genetics Mitochondria - metabolism Mutation Rats Research Resource SciAdv r-resources |
| title | A conditional knockout rat resource of mitochondrial protein-coding genes via a DdCBE-induced premature stop codon |
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