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However, as most infections are still caused by azole-susceptible\n                  <jats:italic>Aspergillus<\/jats:italic>\n                  strains, there is a need to better understand fungal responses to azole antifungals. To this end, we discover that a long non-coding RNA,\n                  <jats:italic>afu-182,<\/jats:italic>\n                  is a major regulator of\n                  <jats:italic>cyp51-<\/jats:italic>\n                  independent sub-MIC azole response. We observe that loss of\n                  <jats:italic>afu-182<\/jats:italic>\n                  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\n                  <jats:italic>afu-182<\/jats:italic>\n                  significantly reduces fungal burden in animals treated with the azole drug, posaconazole. Importantly,\n                  <jats:italic>afu-182<\/jats:italic>\n                  levels decrease upon azole exposure and in an azole adaptation experiment, continuous exposure to low dose azole led to MIC increase in an\n                  <jats:italic>afu-182<\/jats:italic>\n                  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\n                  <jats:italic>afu-182<\/jats:italic>\n                  . 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\n                  <jats:italic>afu-182<\/jats:italic>\n                  in regulating\n                  <jats:italic>Aspergillus fumigatus<\/jats:italic>\n                  response to azole drugs both\n                  <jats:italic>in vitro<\/jats:italic>\n                  and\n                  <jats:italic>in vivo<\/jats:italic>\n                  .\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Importance<\/jats:title>\n                  <jats:p>\n                    Drug resistance in\n                    <jats:italic>Aspergillus<\/jats:italic>\n                    is a major challenge that is often associated with the agricultural use of azoles in the environment. How drug resistance arises\n                    <jats:italic>in vivo<\/jats:italic>\n                    is still an active area of research. Here, we show that azole exposure results in fungal adaptation by lowering the RNA levels of lncRNA, which upon low dose azole exposure leads to an increase in azole drug MIC.\n                  <\/jats:p>\n                <\/jats:sec>","DOI":"10.1101\/2025.10.16.682787","type":"posted-content","created":{"date-parts":[[2025,10,16]],"date-time":"2025-10-16T21:05:39Z","timestamp":1760648739000},"source":"Crossref","is-referenced-by-count":4,"title":["A long non-coding RNA regulates in vitro and in vivo triazole antifungal susceptibility in\n                  <i>Aspergillus fumigatus<\/i>"],"prefix":"10.64898","author":[{"given":"Nava Raj","family":"Poudyal","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, Clemson University, Clemson, SC 29634, USA"},{"name":"Eukaryotic Pathogen Innovation Center, Clemson University, Clemson, SC 29634, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan 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