British scientists use gene editing to investigate what causes miscarriages

Scientists use gene-editing technology to knock out genes in human embryos for first time

The first-of-its-kind study stands in contrast to previous research that attempted to fix disease-causing mutations in human embryos, in the hope of eventually preventing genetic disorders. The findings suggest that weakened OCT4 activity may help explain the cause of some miscarriages, and the reasoning behind why many IVF embryos fail to make it past this critical point in development. However, more studies will be needed to precisely establish the role of this gene.

It's the first time in the world that the technique has been used to help understand the role of genes in early human development. The researchers spent almost a year optimizing techniques in mouse embryos and human stem cells before conducting human embryo experiments, Niakan says. "It's not something that has been possible", he says. "The study is another proof that the findings from experimental animal models can not be always extrapolated to humans".

For the first time in the United Kingdom, researchers have used genome editing technology to examine the function of a specific gene in human embryos.

It is controversial because, say critics, it evokes a future in which humans can order "designer" babies with specific features, perhaps even intelligence. "The processes at work in these embryonic cells will be of interest in many areas of stem cell biology and medicine". Researchers must apply for a license to conduct research, and embryos used for research can not develop for longer than 14 days after fertilization and can not be implanted into a woman's womb.

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In a comment given to the Science Media Centre, Dr Dusko Ilic, a reader in stem-cell science at King's College London, who was not involved in the study said: "One in every four couples has been affected by infertility and to address the issue, we have to understand the biology of the earliest stages of human development".

The researchers disabled OCT4 very early in development. This gene is also known to help human embryonic stem cells stay flexible enough to become any type of body cell, a property known as pluripotency. But researchers didn't know precisely how the OCT4 gene operates during human development. Niakan's team found that human embryos stopped growing earlier than mouse embryos lacking the protein and showed different patterns of gene expression. 80% of the embryos in the test with the gene disabled failed to develop into a blastocyst, which is the stage when the embryos are normally implanted back into the women during in vitro fertilization. There were also unexpected abnormalities in the cells that give rise to the placenta.

Norah Fogarty, first author of the study which is published in Nature, the science journal said -We were surprised to see just how crucial this gene is for human embryo development, but we need to continue our work to confirm its role. As predicted, "knocking out" the OCT4 gene disrupted epiblasts' development.

Dr Ludovic Vallier, study co-author from the Wellcome Trust Sanger Institute and the Wellcome - MRC Cambridge Stem Cell Institute, has said: "This study represents an important step in understanding human embryonic development". "That demonstrates the importance of [studying human embryos]", said Niakan.

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