A long non-coding RNA regulates in vitro and in vivo triazole antifungal susceptibility in Aspergillus fumigatus

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ID: 317319
2026
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Abstract
Azole-resistant Aspergillus infections are a source of increasing concern with limited alternative therapeutic options. However, as most infections are still caused by azole-susceptible Aspergillus strains, there is a need to better understand fungal responses to azole antifungals. To this end, we discover that a long non-coding RNA, afu-182, is a major regulator of cyp51-independent sub-MIC azole response. We observe that loss of afu-182 leads to increased surface attached growth and poor treated disease outcomes in a murine model of invasive pulmonary aspergillosis upon azole treatment. In contrast, overexpression of afu-182 significantly reduces fungal burden in animals treated with the azole drug, posaconazole. Importantly, afu-182 levels decrease upon azole exposure and in an azole adaptation experiment, continuous exposure to low dose azole led to MIC increase in an afu-182 dependent manner. Whole transcriptome analyses revealed that azole drug treatment leads to an increase in transcripts of genes encoding 7-transmembrane domain proteins of the RTA1 family, and these proteins are negatively regulated by afu-182. Two RTA1 family genes have individual and combined effects and are sufficient to increase fungal susceptibility to azole drugs in the WT strain. Taken together, our data show a role of the long non-coding RNA afu-182 in regulating Aspergillus fumigatus response to azole drugs both in vitro and in vivo.
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Authors Nava Raj Poudyal, Ryan Mehlem, Priyanka Doneparthi, T Cady, Garrett Kaufman, Sven D. Willger, Maximiliano Ortiz, Rooksana E. Noorai, Jason Stajich, Sourabh Dhingra
Journal current genetics
Year 2026
DOI
10.1093/genetics/iyag152
URL
https://doi.org/10.1093/genetics/iyag152
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