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Longevity Briefs: Editing Mitochondrial DNA Could Help Us Live Longer

Posted on 17 July 2023

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Longevity briefs provides a short summary of novel research in biology, medicine, or biotechnology that caught the attention of our researchers in Oxford, due to its potential to improve our health, wellbeing, and longevity.

Why is this research important: Mitochondria are the tiny organelles (cellular ‘organs) that produce energy and regulate various cellular processes. Billions of years ago, mitochondria were independent organisms, and still retain some of their own DNA. This mitochondrial DNA (mtDNA) is kept separate from the nuclear DNA that contains most of our genes.

mtDNA is more susceptible to mutations in comparison to the rest of our DNA. Many human diseases, especially those related to ageing, are thought to be related to these mutations. They cause mitochondria to become dysfunctional, promoting accelerated ageing through a variety of mechanisms. Severe disease-causing mutations can also be inherited from mother to child.

Depictions of a healthy (left) and aged, dysfunctional (right) mitochondria.
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If we are ever to reverse the ageing process, it’s possible we will need technologies that can correct mitochondrial mutations in living humans. Unfortunately, existing gene editing tools are not very effective when it comes to targeting mtDNA.

What did the researchers do: In this paper, a team of researchers developed a new method for precise and efficient mtDNA editing, which can change a single nucleotide ‘letter’ (A, T, C or G) without needing to cut the DNA strand. They then tested their method, which they called mitoBEs, in human cells.

Key takeaway(s) from this research:

  • 77% of targeted mtDNA molecules were successfully edited at the targeted letter, and there was little off-target editing.
  • MitoBEs could correct mitochondrial mutations in diseased human mitochondria.
  • In addition to more distant therapeutic benefits, mitochondrial gene editing technology helps us study mitochondrial mutations and their role in ageing.

Researchers achieved up to 77% editing efficiency, meaning that 77% of targeted mtDNA molecules were successfully edited at the targeted letter. The technique also had high specificity, which means that the editing tool did not cause many off-target edits in the nuclear DNA or in parts of the mtDNA outside of the targeted letters. 

They also demonstrated that mitoBEs could correct disease-causing mtDNA mutations in cells taken from patients with mitochondrial diseases, such as Leber hereditary optic neuropathy (LHON), which causes blindness. 

Known hereditary mitochondrial diseases can be prevented by replacing the mitochondria in a fertilised egg with those from a third person. The editing tool developed here brings us a little closer to being able to cure mitochondrial diseases (and eventually age-related mitochondrial dysfunction) in fully developed humans.

A less distant application of this technology is that it will help us learn about mitochondria and how they malfunction during ageing. Gene editing tools like this let researchers mutate mitochondrial genes on purpose, allowing them to better understand their importance in ageing and disease.

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    Strand-selective base editing of human mitochondrial DNA using mitoBEs:

    Title image by Sangharsh Lohakare, Unsplash

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