Long-chain fatty acids promote Candida albicans gut colonization by restructuring the fungal cell surface
Musfirat Shubaita, BS
Advisory Professor: J. Christian Perez, Ph.D.
The yeast Candida albicans is a facultative anaerobe residing in the human digestive tract. Although fungal genetic determinants of mammalian host colonization have been identified, little is known about signals and molecules in the intestinal environment that influence C. albicans proliferation. Previously unpublished data from the Perez lab showed that oleic acid, one of the most abundant long-chain fatty acids in nature, promotes C. albicans colonization of the murine intestine. The goal of this research is to investigate the role of oleic acid in C. albicans gut colonization. I hypothesized that oleic acid promotes, either directly or indirectly, the expression of C. albicans molecules that facilitate the persistence of this fungus in the intestinal domain. I found that β-oxidation, a catabolic process used to break down fatty acids for energy production, was dispensable for C. albicans to colonize mice fed a high-oleic acid diet. Transcriptome analysis revealed that, under anaerobic conditions, oleic acid promoted the expression of several C. albicans transcription factors, which are known to positively regulate intestinal colonization. Furthermore, oleic acid induced the expression of a variety of adhesins and cell surface components. Finally, I identified SOK1 as an oleic acid-induced kinase that dictates cell wall mannan exposure and binding to intestinal mucin under anaerobic conditions. Taken together, these findings indicate that in environments largely void of oxygen (like the colon), dietary oleic acid promotes a C. albicans cell surface configuration that enhances gut occupation.
","abstract_html":"<p><strong>Long-chain fatty acids promote <em>Candida albicans</em> gut colonization by restructuring the fungal cell surface </strong></p> <p>Musfirat Shubaita, BS</p> <p>Advisory Professor: J. Christian Perez, Ph.D.</p> <p>The yeast <em>Candida albicans</em> is a facultative anaerobe residing in the human digestive tract. Although fungal genetic determinants of mammalian host colonization have been identified, little is known about signals and molecules in the intestinal environment that influence <em>C. albicans</em> proliferation. Previously unpublished data from the Perez lab showed that oleic acid, one of the most abundant long-chain fatty acids in nature, promotes <em>C. albicans</em> colonization of the murine intestine. The goal of this research is to investigate the role of oleic acid in <em>C. albicans </em>gut colonization. I hypothesized that oleic acid promotes, either directly or indirectly, the expression of <em>C. albicans</em> molecules that facilitate the persistence of this fungus in the intestinal domain. I found that β-oxidation, a catabolic process used to break down fatty acids for energy production, was dispensable for <em>C. albicans</em> to colonize mice fed a high-oleic acid diet. Transcriptome analysis revealed that, under anaerobic conditions, oleic acid promoted the expression of several <em>C. albicans</em> transcription factors, which are known to positively regulate intestinal colonization. Furthermore, oleic acid induced the expression of a variety of adhesins and cell surface components. Finally, I identified <em>SOK1</em> as an oleic acid-induced kinase that dictates cell wall mannan exposure and binding to intestinal mucin under anaerobic conditions. Taken together, these findings indicate that in environments largely void of oxygen (like the colon), dietary oleic acid promotes a <em>C. albicans</em> cell surface configuration that enhances gut occupation.</p>","abstract_has_math":false,"creators":["Shubaita, Musfirat","Long-chain fatty acids promote Candida albicans gut colonization by restructuring the fungal cell surface
Musfirat Shubaita, BS
Advisory Professor: J. Christian Perez, Ph.D.
The yeast Candida albicans is a facultative anaerobe residing in the human digestive tract. Although fungal genetic determinants of mammalian host colonization have been identified, little is known about signals and molecules in the intestinal environment that influence C. albicans proliferation. Previously unpublished data from the Perez lab showed that oleic acid, one of the most abundant long-chain fatty acids in nature, promotes C. albicans colonization of the murine intestine. The goal of this research is to investigate the role of oleic acid in C. albicans gut colonization. I hypothesized that oleic acid promotes, either directly or indirectly, the expression of C. albicans molecules that facilitate the persistence of this fungus in the intestinal domain. I found that β-oxidation, a catabolic process used to break down fatty acids for energy production, was dispensable for C. albicans to colonize mice fed a high-oleic acid diet. Transcriptome analysis revealed that, under anaerobic conditions, oleic acid promoted the expression of several C. albicans transcription factors, which are known to positively regulate intestinal colonization. Furthermore, oleic acid induced the expression of a variety of adhesins and cell surface components. Finally, I identified SOK1 as an oleic acid-induced kinase that dictates cell wall mannan exposure and binding to intestinal mucin under anaerobic conditions. Taken together, these findings indicate that in environments largely void of oxygen (like the colon), dietary oleic acid promotes a C. albicans cell surface configuration that enhances gut occupation.
"]},{"key":"dc:title","label":"Title","values":["Long-Chain Fatty Acids Promote Candida albicans Gut Colonization by Restructuring the Fungal Cell Surface"]}]}],"canonical_facts":{"dc:contributor":["J. Christian Perez, Ph.D.","Anne Marie Krachler, Ph.D.","Michael C. Lorenz, Ph.D."],"dc:creator":["Shubaita, Musfirat","Long-chain fatty acids promote Candida albicans gut colonization by restructuring the fungal cell surface
Musfirat Shubaita, BS
Advisory Professor: J. Christian Perez, Ph.D.
The yeast Candida albicans is a facultative anaerobe residing in the human digestive tract. Although fungal genetic determinants of mammalian host colonization have been identified, little is known about signals and molecules in the intestinal environment that influence C. albicans proliferation. Previously unpublished data from the Perez lab showed that oleic acid, one of the most abundant long-chain fatty acids in nature, promotes C. albicans colonization of the murine intestine. The goal of this research is to investigate the role of oleic acid in C. albicans gut colonization. I hypothesized that oleic acid promotes, either directly or indirectly, the expression of C. albicans molecules that facilitate the persistence of this fungus in the intestinal domain. I found that β-oxidation, a catabolic process used to break down fatty acids for energy production, was dispensable for C. albicans to colonize mice fed a high-oleic acid diet. Transcriptome analysis revealed that, under anaerobic conditions, oleic acid promoted the expression of several C. albicans transcription factors, which are known to positively regulate intestinal colonization. Furthermore, oleic acid induced the expression of a variety of adhesins and cell surface components. Finally, I identified SOK1 as an oleic acid-induced kinase that dictates cell wall mannan exposure and binding to intestinal mucin under anaerobic conditions. Taken together, these findings indicate that in environments largely void of oxygen (like the colon), dietary oleic acid promotes a C. albicans cell surface configuration that enhances gut occupation.
"],"dc:identifier":["https://digitalcommons.library.tmc.edu/utgsbs_dissertations/1480"],"dc:subject":["Candida albicans","long-chain fatty acids","cell surface","gut colonization","anaerobic","fungal pathogen","Microbial Physiology"],"dc:title":["Long-Chain Fatty Acids Promote Candida albicans Gut Colonization by Restructuring the Fungal Cell Surface"],"thesis:degree_level":["Thesis (MS)"],"thesis:degree_name":["Masters of Science (MS)"]},"updated_at":"2026-07-24T05:49:08Z"}