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Scientists make precise edits to mitochondrial DNA for first time - Nature.com
Jul 08, 2020 1 min, 48 secs

A peculiar bacterial enzyme has allowed researchers to achieve what even the popular CRISPR–Cas9 genome-editing system couldn’t manage: targeted changes to the genomes of mitochondria, cells’ crucial energy-producing structures.

The technique — which builds on a super-precise version of gene editing called base editing — could allow researchers to develop new ways to study, and perhaps even treat, diseases caused by mutations in the mitochondrial genome.

Although there are only a small number of genes in the mitochondrial genome compared with the nuclear genome, these mutations can particularly harm the nervous system and muscles, including the heart, and can be fatal to people who inherit them.

But it has been difficult to study such disorders, because scientists lacked a way to make animal models with the same changes to the mitochondrial genome.

The latest technique marks the first time that researchers have made such targeted changes, and could allow researchers to do this.

“It’s a very exciting development,” says Carlos Moraes, a mitochondrial geneticist at the University of Miami in Florida.

Because of its reliance on the strand of RNA that guides Cas9, this technique wouldn’t be able to reach the mitochondrial genome.

But the enzyme that Mougous’s team had found, called DddA, could act directly on double-stranded DNA without relying on the Cas9 enzyme to break it.

Some countries already allow a procedure called mitochondrial replacement, in which the nucleus of an egg or embryo is transplanted into a donor egg or embryo that contains healthy mitochondria.

Researchers have also been developing a technique to correct mitochondrial mutations by taking advantage of the fact that cells can contain thousands of copies of the mitochondrial genome, and that often, a fraction of these do not contain the mutation linked to disease.

The latest editing approach could allow researchers to correct such mutations even when the mitochondria lack sufficient normal copies of the gene, says Michal Minczuk, a mitochondrial geneticist at the University of Cambridge, UK.

Although medical applications are still distant, researchers will benefit in the short term, he says, by using the technique to generate animal models in which they can study the effects of mitochondrial mutations.

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