Author: Adam Rogers / Source: WIRED
The distant future of designer babies might not seem so distant after all. The last year has been full of news about genetic engineering—much of it driven by the the cut-and-paste technique called Crispr. And at the top of the list: news that Crispr could modify human embryos, correcting a relatively common, often deadly mutation.
The researcher who spearheaded that work in the US, a controversial cell biologist named Shoukhrat Mitalipov, said not only that his team had used Crispr to correct a mutation in a newly fertilized embryo, but that they’d done it via a mechanism that was, if not novel, at least unusual. The response from the scientific community was immediate and negative. They just kinda didn’t buy it. So Wednesday, in the journal Nature—where Mitalipov published the initial work—two groups of researchers published pointed, acronym- and infographic-filled critiques of Mitalipov’s 2017 paper, and Mitalipov attempted to respond. Because the ethics don’t matter—well, not yet—if the science doesn’t actually work.
You know how babies are made, right? Well, Mitalipov’s team didn’t do it that way. Using existing human embryos for scientific research is mostly a no-no in the US, so the scientists took normal human eggs and fertilized them with sperm containing a mutant version of a gene called MYBPC3. That version underlies a disease called hypertrophic cardiomyopathy, the most common cause of sudden death in young athletes. People with two copies of mutant MYBPC3—one from Mom and one from Dad, or homologous for the allele, in the language of genetics—rarely survive childhood. People with just one copy—heterozygous—often have heart problems as they get older.
To try to correct the mutation, Mitalipov’s team used Crispr to cut the mutant gene from the paternal chromosomes and then insert a synthetic, corrected version. But that second step didn’t happen. Instead, according to Mitalipov’s analysis, the cell copied the wild type gene from the maternal chromosomes and inserted that instead. The result: embryos with two wild type alleles. It’s called “homology-dependent repair” or “inter-homolog homologous repair.”
“Some of these authors had been studying DNA repair, and somehow they missed this elephant in the room,” says Mitalipov, the director of the Center for Embryonic Cell and Gene Therapy at Oregon Health and Science University. “We’re pointing to a huge gap in knowledge about how genes repair. We’re not sure if it happens in somatic lineages, but in embryonic lineages, we’ve now proved it.”
Embryologists and cell biologists didn’t think they’d missed an elephant. They didn’t think there was one. “We thought there was an alternative interpretation,” says Paul Thomas, director of SA Genome Editing at the South Australian Health and Medical Research Institute and a lead author of one of the critique articles. Thomas’ work has shown that in mice, Crispr tends to cut…
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