Pronuclear transfer in human embryos to prevent transmission of mitochondrial DNA disease

Lyndsey Craven, Helen A. Tuppen, Gareth D. Greggains, Stephen J. Harbottle, Julie L. Murphy, Lynsey M. Cree, Alison P. Murdoch, Patrick F. Chinnery, Robert W. Taylor, Robert N. Lightowlers, Mary Herbert () and Douglass M. Turnbull ()
Additional contact information
Lyndsey Craven: Mitochondrial Research Group, Institute for Ageing and Health,
Helen A. Tuppen: Mitochondrial Research Group, Institute for Ageing and Health,
Gareth D. Greggains: Newcastle Fertility Centre, International Centre for Life,
Stephen J. Harbottle: Newcastle Fertility Centre, International Centre for Life,
Julie L. Murphy: Mitochondrial Research Group, Institute for Ageing and Health,
Lynsey M. Cree: Mitochondrial Research Group, Institute for Ageing and Health,
Alison P. Murdoch: Newcastle Fertility Centre, International Centre for Life,
Patrick F. Chinnery: Mitochondrial Research Group, Institute for Ageing and Health,
Robert W. Taylor: Mitochondrial Research Group, Institute for Ageing and Health,
Robert N. Lightowlers: Mitochondrial Research Group, Institute for Ageing and Health,
Mary Herbert: Newcastle Fertility Centre, International Centre for Life,
Douglass M. Turnbull: Mitochondrial Research Group, Institute for Ageing and Health,

Nature, 2010, vol. 465, issue 7294, 82-85

Abstract: mtDNA replacement Mitochondrial DNA (mtDNA) mutations passed down from a mother to offspring are a common cause of genetic disease, including neurological, muscle and heart problems, deafness and type 2 diabetes. It was shown recently in non-human primates that nuclear transfer techniques can prevent their transmission. Now, that proof-of-principle work has been extended to human embryos (see News, http://go.nature.com/xqgWXf ). A multi-department team based at Newcastle University transferred pronuclei between human zygotes, and obtained onward development to the blastocyst stage in vitro. Carry-over of donor zygote mtDNA is minimal, so the technique could potentially prevent the transmission of mtDNA disease in humans.

Date: 2010
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DOI: 10.1038/nature08958

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