After seven days, embryo development was stopped and the embryos were analysed.
The central question we are addressing is what are the molecular mechanisms that regulate embryonic stem cell pluripotency and how is it disengaged during cellular differentiation?
The scientists behind it say that it could eventually help understand why some pregnancies fail, and could perhaps one day lead to ways of preventing those failures. According to the results, published today (September 20) in Nature, OCT4 is essential for early embryonic development. The UK Human Fertilisation and Embryology Authority granted permission to do the study - the first time a national regulator has approved research involving gene editing in human embryos (previous studies in other countries were endorsed by local review boards).
The embryos used in the study were donated by couples who had undergone IVF treatment for infertility.
Niakan's team made a decision to use it to stop a key gene from producing a protein called OCT4, which normally becomes active in the first few days of human embryo development. The timer at the bottom right shows how long the embryo has been developing for.
In the study, more than 80 percent of the embryos with the disabled gene failed to develop into a blastocyst, a ball of 200 cells that is the stage when embryos are usually implanted into the womb during in vitro fertilization (IVF). "We would have never gained this insight had we not really studied the function of this gene in human embryos". The work suggests that a protein called OCT4 has additional roles in human embryos compared with those of mice.
"The concerns are that we would be opening the door to fertility clinics vying to offer gene-editing to make future children taller or stronger or whatever they wanted to market", says Marcy Darnovsky, who heads the Center for Genetics and Society, a genetics watchdog group.
The Francis Crick Institute team was only given the go-ahead to conduct the research by the Human Fertilisation and Embryology Authority fertility regulator a year ago. Only about 50% of cells form a blastocyst, she said.
"Now we have demonstrated an efficient way of doing this, we hope that other scientists will use it to find out the roles of other genes".
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"If we knew the key genes that embryos need to develop successfully, we could improve IVF treatments and understand some causes of pregnancy failure", adds lead author Kathy Niakan.
"It may take many years to achieve such an understanding, our study is just the first step", Niakan said.
The study also noted that the expression of OCT4 is different in mice to in humans, affecting the development of the embryo at an earlier stage.
Imagine a world where scientists experiment with the genes of human embryos, turning them on and off to see what happens.
Researchers have traditionally done such studies in mouse embryos, which are more plentiful and carry fewer ethical considerations than human embryos.
The British team's work comes on the heels of milestone science in the United States, where scientists said in July they had succeeded in altering the genes of a human embryo to correct a disease-causing mutation.
They tried unsuccessfully to modify the gene responsible for beta-thalassaemia, a potentially fatal blood disorder, using Crispr/Cas9.
The team used genome editing techniques to stop a key gene from producing a protein called OCT4, which normally becomes active in the first few days of human embryo development.
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