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 Article Writer-   Minakshi  Kumari, MSc. Biotechnology , RCA, Maharana Pratap University of Agriculture and Technology ,Udaipur, Rajsthan(India)

Scientists, at the Broad Institute of MIT and Harvard and the Washington School of Medicine together, developed a method for gene editing of the mitochondrion. They discovered a bacterial toxin called Cytidine deaminase (DddA), having the capability to alter dsDNA while all previously identified Cytidine deaminase enzymes work on ssDNA. DddA changes Cytosine(C) base to Uracil(U).

For many years, many researchers tried to use the CRISPR method of gene editing for mitochondrion editing but remain unsuccessful because this method is applicable only for the nuclear genome. It was ineffective to edit mtDNA because it relies on the entry of guide RNA (gRNA) and there is no way for RNA to enter into mitochondria.

To enable the RNA to enter into mitochondria, scientists split the toxin domain of DddA and attached the TALE protein to their end. Binding of TALE protein to mtDNA brings together and activated the toxin. Now, they exploited the existing protein-import machinery by attaching the amino acid sequence to the construct and acted as a mitochondrial targeting signal.

This method of gene editing could help to cure the diseases due to the mitochondrial genome, like mitochondrial myopathy and Diabetes mellitus and deafness (DAD), in the future.

Reference:

Mok, B. Y. et al. Nature https://10.1038/s41586-020-2477-4 (2020). doi: 10.1038/d41586-020-02054-5