The milestone, revealed in i last week and formally announced tonight, saw scientists demonstrate convincingly for the first time how the defective genes behind hereditary diseases can be corrected in a human embryo.
It worked 72 per cent of the time, in 42 out of 58 embryos.
"The results were encouraging", Arnett said. "This is what we've all been looking for".
Hypertrophic cardiomyopathy is one of more than 10,000 inheritable diseases caused by an error in a single gene, which manifests only in adulthood and affects an estimated one in 500 people. "By using this technique, it's possible to reduce the burden of this heritable disease on the family and eventually the human population", Mitalipov says. It has no cure and can be caused by inheriting just one copy of the bad gene. The healthy embryos were then allowed to grow further - but only for a few days. She said that characteristics that some parents might desire, such as intelligence and athleticism, are influenced by multiple genes and that researchers don't understand all the components of how such characteristics are inherited, much less have the ability to redesign them. The concerns are especially acute when it comes to eggs, sperm and embryos, since changes in these can be passed down to the next generation and forever change the human gene pool.
Science is going through a golden age in editing DNA thanks to a new technology called Crispr, named breakthrough of the year in just 2015. The work conducted by these researchers was well within the guidelines set by the National Academies of Sciences, Engineering, and Medicine on the use of CRISPR to edit human genes. The phenomenon of "mosaicism" (simultaneous presence of genes in healthy and defective in embryo) could not be avoided, the researchers of the new study have been able to do.
But while the procedure is considered to be the first of its kind, human trials are not now allowed in the United States. They were able to correct the defect in an astonishing two thirds of embryos, all without causing a mutation that could prove unsafe. The work was done in the United States for the first time.
"It may be that some countries never permit germline genome editing because of moral and ethical concerns", said Professor Joyce Harper from University College London.
In a surprising discovery, a research team led by Oregon Health and & Science University reported Wednesday that embryos can help fix themselves if scientists jump-start the process early enough.
Instead, Crispr damaged the mutated gene in the father's sperm, leading to a healthy version being copied over from the mother's egg. By comparison, the team found that 13 of 54 treated embryos were mosaics when the CRISPR-Cas9 machinery was injected 18 hours after fertilization.
The researchers co-injected the affected donor's sperm together with the CRISPR editor.
"This technology, independent of the embryos that are there, it would go on and correct all of them".
The scientists in Portland, led by Shoukhrat Mitalipov, said they had successfully edited dozens of embryos. "Whilst there are still some important potential hazards such as mosaicism and off-target effects, substantial progress has been made here on understanding how they might happen and be ameliorated".
Another remarkable finding was the way the repairs to the embryos' faulty DNA took place.
The way Crispr is designed should lead to a new piece of engineered DNA being inserted into the genetic code. "Our program is toward correcting mutant genes". The preferential use of the mother's own template may have something to do with using very early stage embryos. He also noted that there "could be limited situations that could exist where the germ line could be legitimately edited".
In the first successful test of a controversial technique, scientists in a new study were able to edit out heart disease-linked genes from fertilized embryos - with no adverse effects on the cells' other genes.
Not all the embryos were perfectly fixed, though: 16 showed erroneous fixes to their MYBPC3 gene.
Once the defective elements of the gene had been snipped away, the embryo's own cellular fix systems replaced them with healthy versions.
Clearly there is still work to do and debates still to be resolved.
Although arguing the research should prompt a reassessment of whether it would be appropriate to use germline gene editing to treat serious inherited diseases, the researchers stress in no sense should this be viewed as promoting the concept of 'designer babies'.