Antifungal drug resistance evoked via RNAi-dependent epimutations

Silvia Calo, Cecelia Shertz-Wall, Soo Chan Lee, Robert J. Bastidas, Francisco E. Nicolás, Joshua A. Granek, Piotr Mieczkowski, Santiago Torres-Martínez, Rosa M. Ruiz-Vázquez, Maria E. Cardenas and Joseph Heitman ()
Additional contact information
Silvia Calo: Duke University Medical Center
Cecelia Shertz-Wall: Duke University Medical Center
Soo Chan Lee: Duke University Medical Center
Robert J. Bastidas: Duke University Medical Center
Francisco E. Nicolás: Regional Campus of International Excellence “Campus Mare Nostrum”, Murcia 30100, Spain
Joshua A. Granek: Duke University Medical Center
Piotr Mieczkowski: High-Throughput Sequencing Facility, University of North Carolina
Santiago Torres-Martínez: Faculty of Biology, University of Murcia, Murcia 30100, Spain
Rosa M. Ruiz-Vázquez: Faculty of Biology, University of Murcia, Murcia 30100, Spain
Maria E. Cardenas: Duke University Medical Center
Joseph Heitman: Duke University Medical Center

Nature, 2014, vol. 513, issue 7519, 555-558

Abstract: The human fungal pathogen Mucor circinelloides develops spontaneous resistance to an antifungal drug both through mutation and through a newly identified epigenetic RNA-mediated pathway; RNA interference is spontaneously triggered to silence the fkbA gene, giving rise to drug-resistant epimutants that revert to being drug-sensitive once again when grown in the absence of drug.

Date: 2014
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DOI: 10.1038/nature13575

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