Since 1987, the technology surrounding genetic modifications have been associated with CRISPR, an unprecedented tool utilized for altering DNA sequences and functions at the nucleus. Although CRISPR is extraordinarily useful and precise, it limits scientists to DNA in the cell nucleus due to easy allocation via guide RNAs. Recently under the supervision of Joseph Mougous, a professor at the Howard Hughes Medical Institute, and David Liu, a director of the Merkin Institute of Transformative Technologies in Healthcare, Beverly Mok of Harvard University and Marcos de Moraes of the University of Washington published their evolutionary finding: a toxin protein released by Burkholderia cenocepacia. While a bacteria’s weaponry is naturally associated with killing microbes, Burkholderia cenocepacia’s toxin is repurposed. Its original ability of killing bacteria through cytosine-to-uracil conversion in double-stranded DNA is reengineered to perform as a base-editor unreliant on CRISPR or guide RNAs. This breakthrough allows scientists to target mitochondrial mutations at the source, the mitochondria, an organelle untouchable by other technologically advanced genome editors. While CRISPR remains an astounding and valuable facet, this reengineered toxin introduces a new, refreshing method to edit DNA, target mutations, and further study pathways related to drugs and disease.
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