Better Mitochondrial Replacement: But Why?
By Ricki Lewis,
PLOS
| 06. 09. 2016
The disconnect was striking between the headline of the news release a few days ago – “Improved method for mitochondrial replacement therapy” – and the title of the paper to which it refers – “Towards clinical application of pronuclear transfer to prevent mitochondrial DNA disease.”
The news release reported changes in the experimental protocol for pronuclear transfer (PNT) a proposed way to prevent mitochondrial disease. Pronuclei house the genomes in egg and sperm. PNT places them into human fertilized ova whose nuclei have been removed, but whose mitochondria remain in the cytoplasm. The intent is to fashion fertilized ova missing the mitochondria from a woman who has a mitochondrial mutation, which she’d know from having a child with one of the dozen or so diseases caused by mutations in mitochondrial genes. (Additional conditions that affect mitochondria result from mutations in genes in the nucleus).
The paper, published yesterday online in Nature, is from Mary Herbert and colleagues at the Wellcome Trust Centre for Mitochondrial Research, Newcastle upon Tyne, United Kingdom.
It’s a clear, concise report of technically elegant and...
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