Polar bodies are efficient donors for reconstruction of human embryos for potential mitochondrial replacement therapy

In mice, the first （1^st） and second （2^nd） polar bodies （PBs） can be used in place of the female genome of oocytes or zygotes and efficiently support the generation of embryonic stem cells （ESCs） and normal offspring [1- 3]. These results indicate that both Ist and 2nd PBs can be used as nuclear do...

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Published inCell research Vol. 27; no. 8; pp. 1069 - 1072
Main Authors Wu, Keliang, Zhong, Cuiqing, Chen, Tailai, Zhang, Xiaoyu, Tao, Wenrong, Zhang, Jingye, Li, Hongchang, Zhao, Han, Li, Jinsong, Chen, Zi-Jiang
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.08.2017
Nature Publishing Group
Subjects
631/136/1455
692/698/690/1520
692/700/459
692/700/565/1331
Biomedical and Life Sciences
Cell Biology
DNA, Mitochondrial - metabolism
Embryo, Mammalian - metabolism
Embryonic Stem Cells - metabolism
Embryos
Humans
Letter to the Editor
Life Sciences
Mitochondria
Mitochondrial Replacement Therapy
Oocytes - metabolism
Polar Bodies - metabolism
Reconstruction
Zygote - metabolism
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Summary:In mice, the first （1^st） and second （2^nd） polar bodies （PBs） can be used in place of the female genome of oocytes or zygotes and efficiently support the generation of embryonic stem cells （ESCs） and normal offspring [1- 3]. These results indicate that both Ist and 2nd PBs can be used as nuclear donors for mitochondrial replacement therapy （MRT） [4], which is an effective approach for preventing the transmission mitochondria from mother to of disease-causing mutant children [5].
Bibliography:In mice, the first （1^st） and second （2^nd） polar bodies （PBs） can be used in place of the female genome of oocytes or zygotes and efficiently support the generation of embryonic stem cells （ESCs） and normal offspring [1- 3]. These results indicate that both Ist and 2nd PBs can be used as nuclear donors for mitochondrial replacement therapy （MRT） [4], which is an effective approach for preventing the transmission mitochondria from mother to of disease-causing mutant children [5].
31-1568
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ObjectType-Article-2
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These three authors contributed equally to this work.
ISSN:1001-0602
1748-7838
DOI:10.1038/cr.2017.67