This is an audio long read from nature. In this episode, faulty mitochondria caused deadly diseases.

Fixing them is about to get a lot easier. Written by Gemma Conroy and read by me, Benjamin Thompson.

CRISPR gene editing has made its way into every corner of modern biology, but not into every corner of the cell.

Although researchers have used these systems to develop treatments for sickle cell anemia and blood cancers,

to unlock the secrets of multicellularity and to discover the role of thousands of overlooked proteins,

there's one place CRISPR can't easily reach.

Mitochondria

The rings of DNA inside mitochondria are inaccessible to these techniques,

which means that precise edits to mitochondrial DNA, or MT DNA, remain frustratingly out of reach.

Mitochondria missed the CRISPR-Cast-9 revolution that exploded 12 years ago, says Mikhail Minchuk,

a geneticist at the University of Cambridge, UK.

But researchers are eager to access this DNA,

says Minchuk. Mitochondria are bean-shaped organelles that power cells and have myriad other

cellular tasks. Exploring their DNA is essential for understanding the energy production and

exchange that underlies metabolic health.

And more than 300 mutations in this DNA cause mitochondrial diseases.

Incurable genetic disorders with a wide range of symptoms that can rob people of their sight and hearing,

trigger muscle problems and spark seizures.

These disorders affect roughly one in 5,000 people. Because CRISPR can't help with these problems,

researchers have been looking for other ways to precisely edit the mitochondrial genome.

And the past few years have brought some success. The tools are

already proving to be a boon for creating accurate animal models of mitochondrial diseases.

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