Scientists from the Duke University School of Medicine say that they discovered that microorganisms can use a temporary silencing of drug targets, known as epimutations, to gain the benefits of drug resistance without the commitment to permanent mutations. Though the new mechanism was discovered in a fungus called Mucor circinelloides, it is likely to be employed by other fungi as well as bacteria, viruses, and other organisms to withstand treatment with various drugs, according to the researchers.
The team published its study (“Antifungal drug resistance evoked via RNAi-dependent epimutations”) in Nature.
“This mechanism gives the organism more flexibility,” said Joseph Heitman, M.D., Ph.D., senior study author and professor and chair of molecular genetics and microbiology at Duke University School of Medicine. “A classic, Mendelian mutation is a more permanent binding decision. These epimutations are reversible. If conditions change, it is easier to revert to the way things were.”
The epimutations are so transient, in fact, that the researchers almost disregarded them. Cecelia Wall, a graduate student, had been looking for mutations that would make the human fungal pathogen M. circinelloides resistant to the antifungal drug FK506 (also known as tacrolimus). This pathogen causes the rare but lethal fungal infection mucormycosis, an emerging infectious disease that predominantly affects individuals with weakened immune systems.
Read the full, original story: Temporary epimutations confer drug resistance
