Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes

Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are...
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Autor*in:	Mitsutoshi Yamada [verfasserIn] Kazuhiro Akashi [verfasserIn] Reina Ooka [verfasserIn] Kenji Miyado [verfasserIn] Hidenori Akutsu [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Mitochondria DNA (mtDNA), nuclear transfer mitochondria replacement (MR), nDNA–mtDNA compatibility mtDNA–mtDNA compatibility mtDNA replicative segregation mitochondrial function mtDNA genetic drift

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 21(2020), 16, p 5880
Übergeordnetes Werk:	volume:21 ; year:2020 ; number:16, p 5880

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.3390/ijms21165880

Katalog-ID:	DOAJ017268249

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520			\|a Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are a heterogeneous group of inherited disorders with no cure, in which mutated mtDNA is passed from mothers to offspring via maternal egg cytoplasm. Mitochondrial replacement (MR) is a genome transfer technology in which mtDNA carrying disease-related mutations is replaced by presumably disease-free mtDNA. This therapy aims at preventing the transmission of known disease-causing mitochondria to the next generation. Here, a proof of concept for the specific removal or editing of mtDNA disease-related mutations by genome editing is introduced. Although the amount of mtDNA carryover introduced into human oocytes during nuclear transfer is low, the safety of mtDNA heteroplasmy remains a concern. This is particularly true regarding donor-recipient mtDNA mismatch (mtDNA–mtDNA), mtDNA-nuclear DNA (nDNA) mismatch caused by mixing recipient nDNA with donor mtDNA, and mtDNA replicative segregation. These conditions can lead to mtDNA genetic drift and reversion to the original genotype. In this review, we address the current state of knowledge regarding nuclear transplantation for preventing the inheritance of mitochondrial diseases.
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spelling	10.3390/ijms21165880 doi (DE-627)DOAJ017268249 (DE-599)DOAJbd12307f67cf45a58dc715b0fea847a3 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Mitsutoshi Yamada verfasserin aut Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are a heterogeneous group of inherited disorders with no cure, in which mutated mtDNA is passed from mothers to offspring via maternal egg cytoplasm. Mitochondrial replacement (MR) is a genome transfer technology in which mtDNA carrying disease-related mutations is replaced by presumably disease-free mtDNA. This therapy aims at preventing the transmission of known disease-causing mitochondria to the next generation. Here, a proof of concept for the specific removal or editing of mtDNA disease-related mutations by genome editing is introduced. Although the amount of mtDNA carryover introduced into human oocytes during nuclear transfer is low, the safety of mtDNA heteroplasmy remains a concern. This is particularly true regarding donor-recipient mtDNA mismatch (mtDNA–mtDNA), mtDNA-nuclear DNA (nDNA) mismatch caused by mixing recipient nDNA with donor mtDNA, and mtDNA replicative segregation. These conditions can lead to mtDNA genetic drift and reversion to the original genotype. In this review, we address the current state of knowledge regarding nuclear transplantation for preventing the inheritance of mitochondrial diseases. Mitochondria DNA (mtDNA), nuclear transfer mitochondria replacement (MR), nDNA–mtDNA compatibility mtDNA–mtDNA compatibility mtDNA replicative segregation mitochondrial function mtDNA genetic drift Biology (General) Chemistry Kazuhiro Akashi verfasserin aut Reina Ooka verfasserin aut Kenji Miyado verfasserin aut Hidenori Akutsu verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 21(2020), 16, p 5880 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:21 year:2020 number:16, p 5880 https://doi.org/10.3390/ijms21165880 kostenfrei https://doaj.org/article/bd12307f67cf45a58dc715b0fea847a3 kostenfrei https://www.mdpi.com/1422-0067/21/16/5880 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2020 16, p 5880
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allfieldsSound	10.3390/ijms21165880 doi (DE-627)DOAJ017268249 (DE-599)DOAJbd12307f67cf45a58dc715b0fea847a3 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Mitsutoshi Yamada verfasserin aut Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are a heterogeneous group of inherited disorders with no cure, in which mutated mtDNA is passed from mothers to offspring via maternal egg cytoplasm. Mitochondrial replacement (MR) is a genome transfer technology in which mtDNA carrying disease-related mutations is replaced by presumably disease-free mtDNA. This therapy aims at preventing the transmission of known disease-causing mitochondria to the next generation. Here, a proof of concept for the specific removal or editing of mtDNA disease-related mutations by genome editing is introduced. Although the amount of mtDNA carryover introduced into human oocytes during nuclear transfer is low, the safety of mtDNA heteroplasmy remains a concern. This is particularly true regarding donor-recipient mtDNA mismatch (mtDNA–mtDNA), mtDNA-nuclear DNA (nDNA) mismatch caused by mixing recipient nDNA with donor mtDNA, and mtDNA replicative segregation. These conditions can lead to mtDNA genetic drift and reversion to the original genotype. In this review, we address the current state of knowledge regarding nuclear transplantation for preventing the inheritance of mitochondrial diseases. Mitochondria DNA (mtDNA), nuclear transfer mitochondria replacement (MR), nDNA–mtDNA compatibility mtDNA–mtDNA compatibility mtDNA replicative segregation mitochondrial function mtDNA genetic drift Biology (General) Chemistry Kazuhiro Akashi verfasserin aut Reina Ooka verfasserin aut Kenji Miyado verfasserin aut Hidenori Akutsu verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 21(2020), 16, p 5880 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:21 year:2020 number:16, p 5880 https://doi.org/10.3390/ijms21165880 kostenfrei https://doaj.org/article/bd12307f67cf45a58dc715b0fea847a3 kostenfrei https://www.mdpi.com/1422-0067/21/16/5880 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 21 2020 16, p 5880
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source	In International Journal of Molecular Sciences 21(2020), 16, p 5880 volume:21 year:2020 number:16, p 5880
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callnumber-first	Q - Science
author	Mitsutoshi Yamada
spellingShingle	Mitsutoshi Yamada misc QH301-705.5 misc QD1-999 misc Mitochondria DNA (mtDNA), nuclear transfer misc mitochondria replacement (MR), nDNA–mtDNA compatibility misc mtDNA–mtDNA compatibility misc mtDNA replicative segregation misc mitochondrial function misc mtDNA genetic drift misc Biology (General) misc Chemistry Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes
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topic_title	QH301-705.5 QD1-999 Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes Mitochondria DNA (mtDNA), nuclear transfer mitochondria replacement (MR), nDNA–mtDNA compatibility mtDNA–mtDNA compatibility mtDNA replicative segregation mitochondrial function mtDNA genetic drift
topic	misc QH301-705.5 misc QD1-999 misc Mitochondria DNA (mtDNA), nuclear transfer misc mitochondria replacement (MR), nDNA–mtDNA compatibility misc mtDNA–mtDNA compatibility misc mtDNA replicative segregation misc mitochondrial function misc mtDNA genetic drift misc Biology (General) misc Chemistry
topic_unstemmed	misc QH301-705.5 misc QD1-999 misc Mitochondria DNA (mtDNA), nuclear transfer misc mitochondria replacement (MR), nDNA–mtDNA compatibility misc mtDNA–mtDNA compatibility misc mtDNA replicative segregation misc mitochondrial function misc mtDNA genetic drift misc Biology (General) misc Chemistry
topic_browse	misc QH301-705.5 misc QD1-999 misc Mitochondria DNA (mtDNA), nuclear transfer misc mitochondria replacement (MR), nDNA–mtDNA compatibility misc mtDNA–mtDNA compatibility misc mtDNA replicative segregation misc mitochondrial function misc mtDNA genetic drift misc Biology (General) misc Chemistry
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title	Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes
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title_full	Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes
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title_sort	mitochondrial genetic drift after nuclear transfer in oocytes
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title_auth	Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes
abstract	Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are a heterogeneous group of inherited disorders with no cure, in which mutated mtDNA is passed from mothers to offspring via maternal egg cytoplasm. Mitochondrial replacement (MR) is a genome transfer technology in which mtDNA carrying disease-related mutations is replaced by presumably disease-free mtDNA. This therapy aims at preventing the transmission of known disease-causing mitochondria to the next generation. Here, a proof of concept for the specific removal or editing of mtDNA disease-related mutations by genome editing is introduced. Although the amount of mtDNA carryover introduced into human oocytes during nuclear transfer is low, the safety of mtDNA heteroplasmy remains a concern. This is particularly true regarding donor-recipient mtDNA mismatch (mtDNA–mtDNA), mtDNA-nuclear DNA (nDNA) mismatch caused by mixing recipient nDNA with donor mtDNA, and mtDNA replicative segregation. These conditions can lead to mtDNA genetic drift and reversion to the original genotype. In this review, we address the current state of knowledge regarding nuclear transplantation for preventing the inheritance of mitochondrial diseases.
abstractGer	Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are a heterogeneous group of inherited disorders with no cure, in which mutated mtDNA is passed from mothers to offspring via maternal egg cytoplasm. Mitochondrial replacement (MR) is a genome transfer technology in which mtDNA carrying disease-related mutations is replaced by presumably disease-free mtDNA. This therapy aims at preventing the transmission of known disease-causing mitochondria to the next generation. Here, a proof of concept for the specific removal or editing of mtDNA disease-related mutations by genome editing is introduced. Although the amount of mtDNA carryover introduced into human oocytes during nuclear transfer is low, the safety of mtDNA heteroplasmy remains a concern. This is particularly true regarding donor-recipient mtDNA mismatch (mtDNA–mtDNA), mtDNA-nuclear DNA (nDNA) mismatch caused by mixing recipient nDNA with donor mtDNA, and mtDNA replicative segregation. These conditions can lead to mtDNA genetic drift and reversion to the original genotype. In this review, we address the current state of knowledge regarding nuclear transplantation for preventing the inheritance of mitochondrial diseases.
abstract_unstemmed	Mitochondria are energy-producing intracellular organelles containing their own genetic material in the form of mitochondrial DNA (mtDNA), which codes for proteins and RNAs essential for mitochondrial function. Some mtDNA mutations can cause mitochondria-related diseases. Mitochondrial diseases are a heterogeneous group of inherited disorders with no cure, in which mutated mtDNA is passed from mothers to offspring via maternal egg cytoplasm. Mitochondrial replacement (MR) is a genome transfer technology in which mtDNA carrying disease-related mutations is replaced by presumably disease-free mtDNA. This therapy aims at preventing the transmission of known disease-causing mitochondria to the next generation. Here, a proof of concept for the specific removal or editing of mtDNA disease-related mutations by genome editing is introduced. Although the amount of mtDNA carryover introduced into human oocytes during nuclear transfer is low, the safety of mtDNA heteroplasmy remains a concern. This is particularly true regarding donor-recipient mtDNA mismatch (mtDNA–mtDNA), mtDNA-nuclear DNA (nDNA) mismatch caused by mixing recipient nDNA with donor mtDNA, and mtDNA replicative segregation. These conditions can lead to mtDNA genetic drift and reversion to the original genotype. In this review, we address the current state of knowledge regarding nuclear transplantation for preventing the inheritance of mitochondrial diseases.
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title_short	Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes
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Mitochondrial Genetic Drift after Nuclear Transfer in Oocytes

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