Jane Jones, PhD
About Me
Jane earned her bachelor's degree in molecular biology from Colgate University in 2008 before attending the University of Vermont for her graduate work. For her Ph.D. dissertation, Jane's research focused on understanding the role of alternative Nuclear Factor-kappa B signaling in the airway epithelium in the context of allergic inflammation and how this pathway is regulated via redox-dependent mechanisms. After earning her Ph.D. in cellular and molecular biology from the lab of Dr. Yvonne Janssen-Heininger, Jane went on to a post-doctoral fellowship with Dr. Yohannes Tesfaigzi at Lovelace Respiratory Institute in Albuquerque, NM. Jane's research focused on elucidating the roles of Bcl-2 family proteins in the context of allergic inflammation in the airways, specifically focusing on methods to dampen the allergic inflammatory response.
As a research scientist in the Cramer lab, Jane's research focuses on investigating how the current Cystic Fibrosis therapeutic, Trikafta, affects the common pathogenic mold, Aspergillus fumigatus. Excitingly, Jane observed that Trikafta increases the efficacy of two antifungal drugs, Amphotericin B and fksA inhibitor Caspofungin (pictured) by increasing damage to the biofilms. Her research currently focuses on determining the mechanism(s) by which Trikafta improves efficacy of Caspofungin using genetic screening tools, murine models, and multiple in vitro models assessing damage to A. fumigatus biofilms.
In collaboration with graduate student, Katie Quinn, Jane has also been investigating the metabolic requirement for growth and disease initiation of A. fumigatus in the murine lung. Jane and Katie have observed that deletion of the glycolytic gene, phosphofructokinase A (pfkA), prevents initiation of growth and disease in a murine model of aspergillosis, despite being able to grow in carbon sources identified from the lung. Alternatively, deletion of the gluconeogenic gene, acuF, does not impact disease initiation or progression. Taken together these data suggest a critical role for glycolysis in initiating disease, however, recent data suggest that is not all to the story…